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PMC0
bibo:doi
10.1091%2Fmbc.E10-01-0028
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_:vb7705547
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dc:title
introduction
n5:contains
_:vb7705548 _:vb7705549 _:vb7705550 _:vb7705551 _:vb7705560 _:vb7705561 _:vb7705562 _:vb7705563 _:vb7705564 _:vb7705565 _:vb7705566 _:vb7705567 _:vb7705552 _:vb7705553 _:vb7705554 _:vb7705555 _:vb7705556 _:vb7705557 _:vb7705558 _:vb7705559
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_:vb7705548
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Cells either migrate or proliferate, but not both at the same time, a phenomenon termed migration-proliferation dichotomy (Giese et al., >>1996<<; Fedotov and Iomin, 2007).
n2:mentions
n3:8760599
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_:vb7705549
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Cells either migrate or proliferate, but not both at the same time, a phenomenon termed migration-proliferation dichotomy (Giese et al., 1996; Fedotov and Iomin, >>2007<<). This term was initially coined in the context of invading cancer cells, but similar observations were made during development of retinal and tumor blood vessels (Ausprunk and Folkman, 1977; Gerhardt et al., 2003) and epithelial wound
n2:mentions
n3:17501094
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_:vb7705550
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n2:Context
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This term was initially coined in the context of invading cancer cells, but similar observations were made during development of retinal and tumor blood vessels (Ausprunk and Folkman, >>1977<<; Gerhardt et al., 2003) and epithelial wound healing (Gaylarde and Sarkany, 1975; Bonneton et al., 1999; Chung et al., 1999).
n2:mentions
n3:895546
Subject Item
_:vb7705551
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n2:Context
rdf:value
This term was initially coined in the context of invading cancer cells, but similar observations were made during development of retinal and tumor blood vessels (Ausprunk and Folkman, 1977; Gerhardt et al., >>2003<<) and epithelial wound healing (Gaylarde and Sarkany, 1975; Bonneton et al., 1999; Chung et al., 1999).
n2:mentions
n3:12810700
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_:vb7705552
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in the context of invading cancer cells, but similar observations were made during development of retinal and tumor blood vessels (Ausprunk and Folkman, 1977; Gerhardt et al., 2003) and epithelial wound healing (Gaylarde and Sarkany, >>1975<<; Bonneton et al., 1999; Chung et al., 1999). What determines the cellular choice between migration and proliferation has remained unknown.
n2:mentions
n3:1156551
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_:vb7705553
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n2:Context
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cancer cells, but similar observations were made during development of retinal and tumor blood vessels (Ausprunk and Folkman, 1977; Gerhardt et al., 2003) and epithelial wound healing (Gaylarde and Sarkany, 1975; Bonneton et al., >>1999<<; Chung et al., 1999). What determines the cellular choice between migration and proliferation has remained unknown.
n2:mentions
n3:10423270
Subject Item
_:vb7705554
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n2:Context
rdf:value
similar observations were made during development of retinal and tumor blood vessels (Ausprunk and Folkman, 1977; Gerhardt et al., 2003) and epithelial wound healing (Gaylarde and Sarkany, 1975; Bonneton et al., 1999; Chung et al., >>1999<<). What determines the cellular choice between migration and proliferation has remained unknown.
n2:mentions
n3:10440248
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_:vb7705555
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n2:Context
rdf:value
Previous work has established that growth factor receptors such as EGF (Chen et al., 1994a,b), VEGF (Gerhardt et al., 2003), and PDGF (De Donatis et al., 2008) receptors, can trigger both motility and mitosis and that the type and concentration of the activating ligand and the abundance and distribution of receptor influence
n2:mentions
n3:8106552 n3:7962064
Subject Item
_:vb7705556
rdf:type
n2:Context
rdf:value
Previous work has established that growth factor receptors such as EGF (Chen et al., 1994a,b), VEGF (Gerhardt et al., >>2003<<), and PDGF (De Donatis et al., 2008) receptors, can trigger both motility and mitosis and that the type and concentration of the activating ligand and the abundance and distribution of receptor influence whether cells migrate or divide.
n2:mentions
n3:12810700
Subject Item
_:vb7705557
rdf:type
n2:Context
rdf:value
Previous work has established that growth factor receptors such as EGF (Chen et al., 1994a,b), VEGF (Gerhardt et al., 2003), and PDGF (De Donatis et al., >>2008<<) receptors, can trigger both motility and mitosis and that the type and concentration of the activating ligand and the abundance and distribution of receptor influence whether cells migrate or divide.
n2:mentions
n3:18499659
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_:vb7705558
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In proliferating cells, another set of signals (MAP-kinase [MAPK]/ERK1/2, and c-Src/STAT5b) are amplified, which leads to activation of nuclear transcription factors that drive DNA synthesis during mitosis (Haugh, >>2002<<; Kloth et al., 2003).
n2:mentions
n3:14993384
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_:vb7705559
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In proliferating cells, another set of signals (MAP-kinase [MAPK]/ERK1/2, and c-Src/STAT5b) are amplified, which leads to activation of nuclear transcription factors that drive DNA synthesis during mitosis (Haugh, 2002; Kloth et al., >>2003<<). Ligand stimulation initiates both sets of signals, which are rapidly modulated in the immediate postreceptor phase such that migration and mitosis are executed in a mutually exclusive manner (Chen et al., 1994b; De Donatis et al., 2008).
n2:mentions
n3:12429742
Subject Item
_:vb7705560
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Ligand stimulation initiates both sets of signals, which are rapidly modulated in the immediate postreceptor phase such that migration and mitosis are executed in a mutually exclusive manner (Chen et al., 1994b; De Donatis et al., 2008).
n2:mentions
n3:7962064
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_:vb7705561
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n2:Context
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Ligand stimulation initiates both sets of signals, which are rapidly modulated in the immediate postreceptor phase such that migration and mitosis are executed in a mutually exclusive manner (Chen et al., 1994b; De Donatis et al., >>2008<<). Little is known about how cells responding to growth factors make this decision.
n2:mentions
n3:18499659
Subject Item
_:vb7705562
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n2:Context
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Girdin (Garcia-Marcos, et al., >>2009<<). Activation of Gαi by GIV is required for growth factors (EGF and insulin) to trigger cell migration during epithelial wound healing, macrophage chemotaxis, and tumor cell migration (Ghosh et al., 2008).
n2:mentions
n3:19211784
Subject Item
_:vb7705563
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n2:Context
rdf:value
Activation of Gαi by GIV is required for growth factors (EGF and insulin) to trigger cell migration during epithelial wound healing, macrophage chemotaxis, and tumor cell migration (Ghosh et al., >>2008<<). Others implicated GIV/Girdin in development of retinal and tumor blood vessels (Kitamura et al., 2008) and in cancer invasion and metastasis (Jiang et al., 2008) based on its promigratory effects on cells responding to VEGF and
n2:mentions
n3:18663145
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_:vb7705564
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n2:Context
rdf:value
Others implicated GIV/Girdin in development of retinal and tumor blood vessels (Kitamura et al., >>2008<<) and in cancer invasion and metastasis (Jiang et al., 2008) based on its promigratory effects on cells responding to VEGF and insulin-like growth factor (IGF).
n2:mentions
n3:18264090
Subject Item
_:vb7705565
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n2:Context
rdf:value
Others implicated GIV/Girdin in development of retinal and tumor blood vessels (Kitamura et al., 2008) and in cancer invasion and metastasis (Jiang et al., >>2008<<) based on its promigratory effects on cells responding to VEGF and insulin-like growth factor (IGF).
n2:mentions
n3:18316593
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We have shown that the GEF motif within GIV's C terminus, which specifically binds and activates Gαi subunits (Garcia-Marcos et al., >>2009<<, 2010) is the critical component of GIV that is required for cell migration.
n2:mentions
n3:19211784
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_:vb7705567
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Because Gαi and GIV constitute a key regulatory complex within the growth factor signaling network during cell migration (Ghosh et al., >>2008<<), we investigated whether GIV's GEF function and ability to activate Gαi can influence cells to preferentially migrate or proliferate by regulating the EGF receptor (EGFR), the prototype member of the growth factor receptor tyrosine
n2:mentions
n3:18663145
Subject Item
_:vb7705568
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n5:Section
dc:title
materials and methods
n5:contains
_:vb7705572 _:vb7705573 _:vb7705574 _:vb7705575 _:vb7705569 _:vb7705570 _:vb7705571 _:vb7705580 _:vb7705581 _:vb7705582 _:vb7705583 _:vb7705576 _:vb7705577 _:vb7705578 _:vb7705579 _:vb7705584 _:vb7705585 _:vb7705586 _:vb7705587
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_:vb7705569
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Antibodies against GIV that were used in this work include rabbit serum and affinity-purified anti-GIV coiled-coil immunoglobulin (Ig)G (GIV-ccAb) raised against the coiled-coil domain of GIV (Le-Niculescu et al., >>2005<<; Ghosh et al., 2008), and affinity-purified anti-Girdin C terminus (GIV-CTAb) raised against the last 19 aa of GIV's C terminus (IBL America, Minneapolis, MN).
n2:mentions
n3:15749703
Subject Item
_:vb7705570
rdf:type
n2:Context
rdf:value
Antibodies against GIV that were used in this work include rabbit serum and affinity-purified anti-GIV coiled-coil immunoglobulin (Ig)G (GIV-ccAb) raised against the coiled-coil domain of GIV (Le-Niculescu et al., 2005; Ghosh et al., >>2008<<), and affinity-purified anti-Girdin C terminus (GIV-CTAb) raised against the last 19 aa of GIV's C terminus (IBL America, Minneapolis, MN).
n2:mentions
n3:18663145
Subject Item
_:vb7705571
rdf:type
n2:Context
rdf:value
To visualize total EGFR by immunofluorescence, mAb #225 raised against the ectodomain (gift from Gordon Gill, University of California San Diego [UCSD], La Jolla, CA; Gill et al., >>1984<<) or polyclonal antibody (pAb) anti-EGFR against the C-terminus of EGFR (Cell Signaling Technology).
n2:mentions
n3:6330079
Subject Item
_:vb7705572
rdf:type
n2:Context
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Rockman (Duke University Medical Center, Durham, NC) (Noma et al., >>2007<<). Cloning of Gαi3 and GIV into pGEX-4T-1 or pET28b were described previously (Garcia-Marcos et al., 2009).
n2:mentions
n3:17786238
Subject Item
_:vb7705573
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n2:Context
rdf:value
Cloning of Gαi3 and GIV into pGEX-4T-1 or pET28b were described previously (Garcia-Marcos et al., >>2009<<). To transiently express C-terminal FLAG-tagged Gαi3 in Cos7 cells, Gαi3 was cloned into p3XFLAG-CMVTM-14 expression vector using BamHI and HindIII restriction enzymes. Expression and purification of His-GIV-CT (1623–1870) were done as
n2:mentions
n3:19211784
Subject Item
_:vb7705574
rdf:type
n2:Context
rdf:value
Expression and purification of His-GIV-CT (1623–1870) were done as described previously (Garcia-Marcos et al., >>2009<<). GIV and Gαi3 mutants were generated using specific primers (sequences available upon request) following the manufacturer's instructions (QuikChange II; Stratagene, La Jolla, CA). The truncated GIVΔCT construct was generated by creating
n2:mentions
n3:19211784
Subject Item
_:vb7705575
rdf:type
n2:Context
rdf:value
RNA interference (RNAi)-resistant GIV was generated by silent mutations as described previously (Enomoto et al., >>2005<<). To obtain glutathione transferase (GST)-tagged cytoplasmic tail of EGFR (GST-EGFR-T), EGFR cDNA (encoding aa 1046–1210) was amplified by polymerase chain reaction (PCR) and cloned into pGEX4T3 using EcoRI and XhoI sites. All constructs
n2:mentions
n3:16139227
Subject Item
_:vb7705576
rdf:type
n2:Context
rdf:value
Plasmids encoding GST-Gαi3, GST-EGFR, His-Gαi3, or His-GIV-CT fusion constructs were used to express these proteins in Escherichia coli exactly as described previously (Ghosh et al., >>2008<<; Garcia-Marcos et al., 2009, 2010).
n2:mentions
n3:18663145
Subject Item
_:vb7705577
rdf:type
n2:Context
rdf:value
Plasmids encoding GST-Gαi3, GST-EGFR, His-Gαi3, or His-GIV-CT fusion constructs were used to express these proteins in Escherichia coli exactly as described previously (Ghosh et al., 2008; Garcia-Marcos et al., >>2009<<, 2010).
n2:mentions
n3:19211784
Subject Item
_:vb7705578
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The 21T breast cell lines (16N, NT, and MT2) were obtained from Arthur Pardee (Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA) and maintained as described previously (Band et al., >>1990<<; Qiao et al., 2007).
n2:mentions
n3:1977518
Subject Item
_:vb7705579
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The 21T breast cell lines (16N, NT, and MT2) were obtained from Arthur Pardee (Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA) and maintained as described previously (Band et al., 1990; Qiao et al., >>2007<<). Ls-174T and Ls-LiM6 were obtained from Robert Bresalier (The University of Texas MD Anderson Cancer Center, Houston, TX) and grown as described previously (Bresalier et al., 1987). Ls-174T is a poorly metastatic colon cancer cell line
n2:mentions
n3:17545609
Subject Item
_:vb7705580
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Ls-174T and Ls-LiM6 were obtained from Robert Bresalier (The University of Texas MD Anderson Cancer Center, Houston, TX) and grown as described previously (Bresalier et al., >>1987<<). Ls-174T is a poorly metastatic colon cancer cell line harvested from a Duke's clinical stage B tumor. Ls-LiM6 is a highly metastatic subclone of Ls-174T cells that was selected by serial passage of Ls-174T through a murine
n2:mentions
n3:3028609
Subject Item
_:vb7705581
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Transfections to transiently overexpress proteins using FLAG-EGFR, GIV-NT, or Gαi3 plasmids or protein silencing using siRNA Gαi3 were carried out exactly as described previously (Garcia-Marcos et al., >>2009<<). HeLa cell lines stably expressing GIV-wt (HeLa-GIV-wt) or GIV-F1685A mutant (HeLa-GIV-FA) were generated as described previously (Garcia-Marcos et al., 2009). A HeLa cell line stably expressing GIV 1-1354 (GIVΔCT) was generated using
n2:mentions
n3:19211784
Subject Item
_:vb7705582
rdf:type
n2:Context
rdf:value
HeLa cell lines stably expressing GIV-wt (HeLa-GIV-wt) or GIV-F1685A mutant (HeLa-GIV-FA) were generated as described previously (Garcia-Marcos et al., >>2009<<). A HeLa cell line stably expressing GIV 1-1354 (GIVΔCT) was generated using the same protocol. All these cell lines were maintained in the presence of G418 (500 μg/ml, Cellgro, Mediatech, Herndon, VA). Clones were chosen for each
n2:mentions
n3:19211784
Subject Item
_:vb7705583
rdf:type
n2:Context
rdf:value
Experiments on cells expressing Gαi3-yellow fluorescent protein (YFP) were performed as described previously (Ghosh et al., >>2008<<). For study of GIV-wt and GIV-FA HeLa cells serum was reduced to 0.2%, and after 6–12 h cells were scratch wounded with a 20-μl pipette tip and 0.1 nM EGF was added. Cells were immediately transferred to an incubated stage (37°C in 5%
n2:mentions
n3:18663145
Subject Item
_:vb7705584
rdf:type
n2:Context
rdf:value
Cells were fixed at room temperature with 3% paraformaldehyde for 30 min, permeabilized (0.2% Triton X-100) for 45 min, and incubated for 1 h each with primary and then secondary antibodies as described previously (Ghosh et al., >>2008<<). Antibody dilutions were as follows: affinity-purified GIV (ccAb), 1:30; Gαi3 (Calbiochem), 1:
n2:mentions
n3:18663145
Subject Item
_:vb7705585
rdf:type
n2:Context
rdf:value
For surface labeling of EGFR (see Figure 3A), HRP-conjugated EGF was generated by incubating 5 μg Strep-HRP with 0.3 μg biotinylated-EGF in 300 μl PBS overnight at 4C as described previously (Razi and Futter, >>2006<<). Ligand-bound receptor was then visualized using Rhodamine-Red X anti-HRP (1:100; Jackson ImmunoResearch Laboratories). Images were acquired with an Axioimager M1 microscope using a 100× aperture (Plan Neofluar, 1.30 numerical aperture
n2:mentions
n3:16707569
Subject Item
_:vb7705586
rdf:type
n2:Context
rdf:value
The in vitro binding assays using GST-fusion proteins were carried out as described previously (Ghosh et al., >>2008<<). In brief, purified GST-fusion proteins (15–20 μg) or GST alone (30 μg) were immobilized on glutathione-Sepharose beads and resuspended in binding buffer supplemented with nucleotides (50 mM Tris-HCl, pH 7.4, 100 mM NaCl, 0.4% [vol/vol],
n2:mentions
n3:18663145
Subject Item
_:vb7705587
rdf:type
n2:Context
rdf:value
pH 7.4, 100 mM NaCl, 0.4% [vol/vol], NP-40, 10 mM MgCl2, 5 mM EDTA, 2 mM DTT, and protease inhibitor cocktail supplemented with either 30 μM GDP or 30 μM guanosine diphosphate [GDP], 30 μM AlCl3, and 10 mM NaF) (Ghosh et al., >>2008<<). Thereafter, [35S]Met (GE Healthcare) -labeled GIV prepared using the TnT Quick Coupled Transcription/Translation System (Promega, Madison, WI) was added to the binding buffer, and binding was carried out overnight at 4°C with constant
n2:mentions
n3:18663145
Subject Item
_:vb7705588
rdf:type
n5:Section
dc:title
results
n5:contains
_:vb7705620 _:vb7705621 _:vb7705622 _:vb7705623 _:vb7705616 _:vb7705617 _:vb7705618 _:vb7705619 _:vb7705624 _:vb7705625 _:vb7705604 _:vb7705605 _:vb7705606 _:vb7705607 _:vb7705600 _:vb7705601 _:vb7705602 _:vb7705603 _:vb7705612 _:vb7705613 _:vb7705614 _:vb7705615 _:vb7705608 _:vb7705609 _:vb7705610 _:vb7705611 _:vb7705589 _:vb7705590 _:vb7705591 _:vb7705596 _:vb7705597 _:vb7705598 _:vb7705599 _:vb7705592 _:vb7705593 _:vb7705594 _:vb7705595
Subject Item
_:vb7705589
rdf:type
n2:Context
rdf:value
the behavior of HeLa cells stably expressing either siRNA-resistant wild-type GIV (GIV-wt cells) or a GEF-deficient GIV F1685A mutant (GIV-FA cells) incapable of interacting with or activating the G protein (Garcia-Marcos et al., >>2009<<). Endogenous GIV was depleted in both cell lines using previously validated siRNA oligonucleotides (Enomoto et al., 2005; Ghosh et al., 2008).
n2:mentions
n3:19211784
Subject Item
_:vb7705590
rdf:type
n2:Context
rdf:value
Endogenous GIV was depleted in both cell lines using previously validated siRNA oligonucleotides (Enomoto et al., >>2005<<; Ghosh et al., 2008).
n2:mentions
n3:16139227
Subject Item
_:vb7705591
rdf:type
n2:Context
rdf:value
Endogenous GIV was depleted in both cell lines using previously validated siRNA oligonucleotides (Enomoto et al., 2005; Ghosh et al., >>2008<<). Cells were stimulated with EGF in combination with scratch wounding, and both migration and proliferation at the wound edge were simultaneously monitored by live cell imaging. We found that GIV-wt cells typically migrated into the
n2:mentions
n3:18663145
Subject Item
_:vb7705592
rdf:type
n2:Context
rdf:value
The mitotic index as determined by levels of phospho-histone H3, an indicator of mitosis (Hans and Dimitrov, >>2001<<), was consistently high in GIV-FA cells, intermediate in control (untransfected) cells, and low in GIV-wt cells after scratch wounding (Supplemental Figure S2, A and B).
n2:mentions
n3:11420717
Subject Item
_:vb7705593
rdf:type
n2:Context
rdf:value
HeLa cells transfected with Gαi3wt-YFP, Gαi3(QL)-YFP, or Gi3(GA)-YFP were grown to confluence and stimulated by scratch wounding in the presence of 10% serum to initiate EGFR signaling (Tetreault et al., >>2007<<). Cells were then imaged for 8 h as they migrated into the wound (see Supplemental Movies 3 and 4; as in A). Bar graphs display the percent of cells at the edge of the wound that migrate or divide. Results are shown as mean ± SEM (n =
n2:mentions
n3:17708540
Subject Item
_:vb7705594
rdf:type
n2:Context
rdf:value
Because GIV-wt and GIV-FA cells differ by a single point mutation that specifically disrupts GIV's GEF activity and prevents activation of Gαi3 (Garcia-Marcos et al., >>2009<<), we asked whether G protein activity alone is sufficient to create this phenotypic dichotomy.
n2:mentions
n3:19211784
Subject Item
_:vb7705595
rdf:type
n2:Context
rdf:value
We stimulated HeLa cells expressing YFP-tagged Gαi3-wt or the constitutively inactive Gαi3-G203A (GA) or active (GTPase-deficient) Gαi3-Q204L (QL) mutant (Hermouet et al., >>1991<<) by scratch wounding, and then we monitored cell motility and division simultaneously by live cell imaging.
n2:mentions
n3:1660138
Subject Item
_:vb7705596
rdf:type
n2:Context
rdf:value
GIV-wt, GIV-FA, and control HeLa cells were stimulated with EGF and analyzed by immunoblotting for activation (phosphorylation) of four major EGFR-stimulated signals—Akt, PLCγ1, ERK1/2 MAPK, and c-Src/STAT5b (Haugh, >>2002<<; Kloth et al., 2003).
n2:mentions
n3:14993384
Subject Item
_:vb7705597
rdf:type
n2:Context
rdf:value
GIV-FA, and control HeLa cells were stimulated with EGF and analyzed by immunoblotting for activation (phosphorylation) of four major EGFR-stimulated signals—Akt, PLCγ1, ERK1/2 MAPK, and c-Src/STAT5b (Haugh, 2002; Kloth et al., >>2003<<). GIV-wt cells showed enhanced Akt and PLCγ1 phosphorylation but attenuated STAT5b and ERK1/2 phosphorylation, whereas GIV-FA cells showed the opposite, i.e., enhanced ERK1/2 and STAT5b but attenuated Akt and PLCγ1 signaling (Figure 1, C
n2:mentions
n3:12429742
Subject Item
_:vb7705598
rdf:type
n2:Context
rdf:value
c-Src activity, as determined by dephosphorylation of pY527 on Src, which coincides with entry into mitosis (Bagrodia et al., >>1991<<), was decreased in GIV-wt and increased in GIV-FA cells compared with controls (Figure 1, C and D).
n2:mentions
n3:1702522
Subject Item
_:vb7705599
rdf:type
n2:Context
rdf:value
We conclude that GIV's C-terminal GEF motif, which activates Gαi (Garcia-Marcos et al., >>2009<<), is the critical component of the decision to migrate or proliferate.
n2:mentions
n3:19211784
Subject Item
_:vb7705600
rdf:type
n2:Context
rdf:value
EGFR signaling to downstream effectors is mediated through ligand-induced tyrosine autophosphorylation of the EGFR tail and SH2 adaptor recruitment to the resultant phosphotyrosines (Schlessinger, >>2002<<). We next investigated whether GIV's GEF activity regulates these two early events in EGFR signaling.
n2:mentions
n3:12297041
Subject Item
_:vb7705601
rdf:type
n2:Context
rdf:value
were stimulated with EGF, and EGFR autophosphorylation was assessed at Y992, Y1045, and Y1068, (docking sites of the SH2 adaptors, PLCγ1, cCbl, and Grb2) and at Y845 (the substrate for c-Src kinase that triggers mitosis; Tice et al., >>1999<<), using site-specific phospho-Tyr antibodies (Figure 2A).
n2:mentions
n3:9990038
Subject Item
_:vb7705602
rdf:type
n2:Context
rdf:value
The distribution of ligand-activated EGFR between the plasma membrane (PM) and endosomes is known to affect EGFR signaling (Haugh, >>2002<<) in that motogenic PI3K and PLCγ signals are initiated by ligand-activated receptor largely or exclusively at the PM, whereas mitogenic MAPK-ERK1/2 and c-Src signals can be propagated from endosomes (Murphy et al., 2009).
n2:mentions
n3:14993384
Subject Item
_:vb7705603
rdf:type
n2:Context
rdf:value
(Haugh, 2002) in that motogenic PI3K and PLCγ signals are initiated by ligand-activated receptor largely or exclusively at the PM, whereas mitogenic MAPK-ERK1/2 and c-Src signals can be propagated from endosomes (Murphy et al., >>2009<<). To find out whether the different signaling profiles we observed in GIV-wt and GIV-FA cells are accompanied by differences in distribution of EGFR we compared the localization of ligand-bound EGFR in GIV-wt and GIV-FA cells.
n2:mentions
n3:19822761
Subject Item
_:vb7705604
rdf:type
n2:Context
rdf:value
Cell surface EGFR was labeled in chilled (4°C), serum-starved cells using HRP-tagged EGF (Razi and Futter, >>2006<<), after which cells were warmed to 37°C for 15 min and then fixed and analyzed for the distribution of the ligand (HRP-EGF)-bound receptor by immunofluorescence.
n2:mentions
n3:16707569
Subject Item
_:vb7705605
rdf:type
n2:Context
rdf:value
To establish the nature of these compartments, we costained HRP-EGF (Figure 3B, a–c) or EGFR [using anti-EGFR mAb; Burke et al., >>2001<<)] (Figure 3Bd) with markers of early (EEA1) or late (CI-MPR; data not shown) endosomes.
n2:mentions
n3:11408594
Subject Item
_:vb7705606
rdf:type
n2:Context
rdf:value
Gαi3-3XFLAG (lane 6), which is known to interact with GIV-CT (Garcia-Marcos et al., >>2009<<), was used as a positive control.
n2:mentions
n3:19211784
Subject Item
_:vb7705607
rdf:type
n2:Context
rdf:value
By contrast, GIV-CT (aa 1623–1870), which contains the crucial actin binding (Enomoto et al., >>2005<<) and GEF (Garcia-Marcos et al., 2009) domains, bound only after EGF stimulation (Figure 4E, lane 5).
n2:mentions
n3:16139227
Subject Item
_:vb7705608
rdf:type
n2:Context
rdf:value
By contrast, GIV-CT (aa 1623–1870), which contains the crucial actin binding (Enomoto et al., 2005) and GEF (Garcia-Marcos et al., >>2009<<) domains, bound only after EGF stimulation (Figure 4E, lane 5).
n2:mentions
n3:19211784
Subject Item
_:vb7705609
rdf:type
n2:Context
rdf:value
EGFR signaling has been implicated in the generation of migration-proliferation dichotomy during cancer invasion (Athale et al., >>2005<<). Previously, we demonstrated that GIV's GEF function is required for the prometastatic properties of cancer cells (Garcia-Marcos et al., 2009) and that full-length GIV (GIV-fl) is expressed in some but not all cancer cells (Ghosh et al.,
n2:mentions
n3:15748909
Subject Item
_:vb7705610
rdf:type
n2:Context
rdf:value
Previously, we demonstrated that GIV's GEF function is required for the prometastatic properties of cancer cells (Garcia-Marcos et al., >>2009<<) and that full-length GIV (GIV-fl) is expressed in some but not all cancer cells (Ghosh et al., 2008).
n2:mentions
n3:19211784
Subject Item
_:vb7705611
rdf:type
n2:Context
rdf:value
we demonstrated that GIV's GEF function is required for the prometastatic properties of cancer cells (Garcia-Marcos et al., 2009) and that full-length GIV (GIV-fl) is expressed in some but not all cancer cells (Ghosh et al., >>2008<<). Here, we investigated whether the presence or absence of GIV's GEF function differentiates slow growing, highly motile colon cancer cells from rapidly growing, poorly motile cells.
n2:mentions
n3:18663145
Subject Item
_:vb7705612
rdf:type
n2:Context
rdf:value
an antibody against the C-terminal 19 aa of GIV, we detected GIV-fl (∼250 kDa) in slowly growing highly motile/highly invasive (DLD1 and HCT-116) cells but not in rapidly growing poorly motile colon cancer cells (Lelievre et al., >>1998<<; Brattain et al., 1999) with low invasiveness (HT29 and LS174T) (Figure 5A).
n2:mentions
n3:9543252
Subject Item
_:vb7705613
rdf:type
n2:Context
rdf:value
Similar results were obtained on three breast cancer cell lines with different growth and invasive potential (Howlin et al., >>2008<<): GIV-fl (protein and mRNA) was expressed only in slow-growing, highly motile/invasive cells and undetectable in fast-growing, poorly motile cells with low invasiveness (Figure 5B), whereas levels of Gαi3 were equal. In contrast, a GIV-fl
n2:mentions
n3:18435854
Subject Item
_:vb7705614
rdf:type
n2:Context
rdf:value
cells is wild-type in sequence and that the translated protein selectively binds Gαi3 in the presence of GDP, but not GDP · AlF4− (data not shown), indicating that GIV retains its properties as a nonreceptor GEF (Garcia-Marcos et al., >>2009<<). These results indicate that altered expression of GIV, but not Gαi3, is the key feature that determines whether a functional complex can be assembled in vivo:
n2:mentions
n3:19211784
Subject Item
_:vb7705615
rdf:type
n2:Context
rdf:value
Because metastasis-related genes often undergo alternative splicing leading to aberrant expression (Weber, >>2008<<; Srebrow and Kornblihtt, 2006), we asked whether dysregulation of GIV-fl expression occurs due to alternative splicing.
n2:mentions
n3:18522865
Subject Item
_:vb7705616
rdf:type
n2:Context
rdf:value
Because metastasis-related genes often undergo alternative splicing leading to aberrant expression (Weber, 2008; Srebrow and Kornblihtt, >>2006<<), we asked whether dysregulation of GIV-fl expression occurs due to alternative splicing.
n2:mentions
n3:16787944
Subject Item
_:vb7705617
rdf:type
n2:Context
rdf:value
These results indicate that in poorly invasive cells, IR effectively disrupted translation resulting in down-regulation of GIV-fl expression, a phenomenon known to occur in other instances during oncogenesis (Dreyfuss et al., >>2002<<).
n2:mentions
n3:11994740
Subject Item
_:vb7705618
rdf:type
n2:Context
rdf:value
GIV-fl bound Gαi3 preferentially in the presence of GDP as shown previously (Garcia-Marcos et al., >>2009<<), whereas GEF-deficient GIVΔCT showed no binding.
n2:mentions
n3:19211784
Subject Item
_:vb7705619
rdf:type
n2:Context
rdf:value
Although GIV-fl was undetectable using GIV-CTAb that recognizes the C terminus (Figure 5, A and B), a ∼135-kDa protein was detected with GIV-cc antibody which recognizes the N-terminal coiled-coil domain (Le-Niculescu et al., >>2005<<; Figure 6D) indicating that this variant lacks the C-terminus (GIVΔCT).
n2:mentions
n3:15749703
Subject Item
_:vb7705620
rdf:type
n2:Context
rdf:value
We assessed if GIVΔCT, which lacks the C-terminal GEF motif (Garcia-Marcos et al., >>2009<<), could bind Gαi3 in a pull-down assay, and, as anticipated, GIVΔCT did not bind Gαi3 in vitro (Figure 6E); therefore, it is incapable of assembling a functional complex with Gαi3 in vivo.
n2:mentions
n3:19211784
Subject Item
_:vb7705621
rdf:type
n2:Context
rdf:value
Next, we investigated whether alternative splicing of GIV's C terminus takes place in tumors in vivo during cancer invasion—a process that relies heavily on EGFR signaling (Wells et al., >>2002<<). We carried out immunohistochemistry (IHC) for GIV on paraffin-embedded human colorectal cancers representing various stages of invasive disease (Duke's stages A through D, where A denotes locally restricted tumor without spread and D
n2:mentions
n3:12102155
Subject Item
_:vb7705622
rdf:type
n2:Context
rdf:value
In keeping with the previously reported high expression of GIV-fl in mesenchymal cells (Enomoto et al., >>2005<<; Ghosh et al., 2008; Jiang et al., 2008; Kitamura et al., 2008), the stroma stained very strongly in both normal and cancer tissues (Figure 7A and Supplemental Figure S7b).
n2:mentions
n3:16139227
Subject Item
_:vb7705623
rdf:type
n2:Context
rdf:value
In keeping with the previously reported high expression of GIV-fl in mesenchymal cells (Enomoto et al., 2005; Ghosh et al., >>2008<<; Jiang et al., 2008; Kitamura et al., 2008), the stroma stained very strongly in both normal and cancer tissues (Figure 7A and Supplemental Figure S7b).
n2:mentions
n3:18663145
Subject Item
_:vb7705624
rdf:type
n2:Context
rdf:value
In keeping with the previously reported high expression of GIV-fl in mesenchymal cells (Enomoto et al., 2005; Ghosh et al., 2008; Jiang et al., >>2008<<; Kitamura et al., 2008), the stroma stained very strongly in both normal and cancer tissues (Figure 7A and Supplemental Figure S7b).
n2:mentions
n3:18316593
Subject Item
_:vb7705625
rdf:type
n2:Context
rdf:value
In keeping with the previously reported high expression of GIV-fl in mesenchymal cells (Enomoto et al., 2005; Ghosh et al., 2008; Jiang et al., 2008; Kitamura et al., >>2008<<), the stroma stained very strongly in both normal and cancer tissues (Figure 7A and Supplemental Figure S7b).
n2:mentions
n3:18264090
Subject Item
_:vb7705626
rdf:type
n5:Section
dc:title
discussion
n5:contains
_:vb7705628 _:vb7705629 _:vb7705630 _:vb7705631 _:vb7705627 _:vb7705644 _:vb7705645 _:vb7705646 _:vb7705647 _:vb7705640 _:vb7705641 _:vb7705642 _:vb7705643 _:vb7705636 _:vb7705637 _:vb7705638 _:vb7705639 _:vb7705632 _:vb7705633 _:vb7705634 _:vb7705635 _:vb7705660 _:vb7705661 _:vb7705662 _:vb7705663 _:vb7705656 _:vb7705657 _:vb7705658 _:vb7705659 _:vb7705652 _:vb7705653 _:vb7705654 _:vb7705655 _:vb7705648 _:vb7705649 _:vb7705650 _:vb7705651 _:vb7705664
Subject Item
_:vb7705627
rdf:type
n2:Context
rdf:value
By contrast, GIV-FA cells or GIVΔCT cells that express GEF-deficient variants of GIV, which are defective in their ability to interact with or activate Gαi (Garcia-Marcos et al., >>2009<<), frequently divide but rarely migrate.
n2:mentions
n3:19211784
Subject Item
_:vb7705628
rdf:type
n2:Context
rdf:value
Previous work predicted a central role for EGFR in migration-proliferation dichotomy (Athale et al., >>2005<<) and demonstrated that the signaling pathways that lead to motility or cell proliferation diverge at the immediate postreceptor phase (Chen et al., 1994b).
n2:mentions
n3:15748909
Subject Item
_:vb7705629
rdf:type
n2:Context
rdf:value
a central role for EGFR in migration-proliferation dichotomy (Athale et al., 2005) and demonstrated that the signaling pathways that lead to motility or cell proliferation diverge at the immediate postreceptor phase (Chen et al., 1994b). We have defined the point of divergence by showing that when GIV is able to bind to the EGFR tail and activate Gαi cells are biased to migrate.
n2:mentions
n3:7962064
Subject Item
_:vb7705630
rdf:type
n2:Context
rdf:value
Our finding that G protein activity plays a key role in orchestrating this migration-proliferation dichotomy is also consistent with previous work demonstrating that migration is triggered by active Gαi3 (Ghosh et al., >>2008<<), but mitosis is enhanced by inactive Gαi (Cho and Kehrl, 2007).
n2:mentions
n3:18663145
Subject Item
_:vb7705631
rdf:type
n2:Context
rdf:value
role in orchestrating this migration-proliferation dichotomy is also consistent with previous work demonstrating that migration is triggered by active Gαi3 (Ghosh et al., 2008), but mitosis is enhanced by inactive Gαi (Cho and Kehrl, >>2007<<). We conclude that both G protein and growth factor signaling operate through GIV and participate in establishing migration-proliferation dichotomy and that the presence or absence of GIV-dependent Gαi activation is crucial for it to take
n2:mentions
n3:17635935
Subject Item
_:vb7705632
rdf:type
n2:Context
rdf:value
The nonselective suppression of signals we observe in cells without GIV may also explain why these cells were characterized previously as growth deficient and immotile (Anai et al., >>2005<<; Enomoto et al., 2005).
n2:mentions
n3:15753085
Subject Item
_:vb7705633
rdf:type
n2:Context
rdf:value
The nonselective suppression of signals we observe in cells without GIV may also explain why these cells were characterized previously as growth deficient and immotile (Anai et al., 2005; Enomoto et al., >>2005<<). Similarly, we have shown that without Gαi, GIV-dependent signaling and cell migration are inhibited (Ghosh et al., 2008), and cells are rendered proapoptotic (Ohman et al., 2002). We conclude that both Gαi and GIV are required for cell
n2:mentions
n3:16139227
Subject Item
_:vb7705634
rdf:type
n2:Context
rdf:value
Similarly, we have shown that without Gαi, GIV-dependent signaling and cell migration are inhibited (Ghosh et al., >>2008<<), and cells are rendered proapoptotic (Ohman et al., 2002).
n2:mentions
n3:18663145
Subject Item
_:vb7705635
rdf:type
n2:Context
rdf:value
Similarly, we have shown that without Gαi, GIV-dependent signaling and cell migration are inhibited (Ghosh et al., 2008), and cells are rendered proapoptotic (Ohman et al., >>2002<<). We conclude that both Gαi and GIV are required for cell migration and mitosis, however, activation of Gαi by GIV biases the cells to migrate.
n2:mentions
n3:12171962
Subject Item
_:vb7705636
rdf:type
n2:Context
rdf:value
Indirect stimulation of growth factor receptors by GPCR/G protein intermediates—so-called transactivation—is well established (Luttrell et al., >>1999<<). Signaling via G proteins after direct stimulation of growth factor receptors has also been described previously (Waters et al., 2004; Dhanasekaran, 2006), but there is little mechanistic insight into how this could occur.
n2:mentions
n3:10209148
Subject Item
_:vb7705637
rdf:type
n2:Context
rdf:value
Signaling via G proteins after direct stimulation of growth factor receptors has also been described previously (Waters et al., >>2004<<; Dhanasekaran, 2006), but there is little mechanistic insight into how this could occur.
n2:mentions
n3:15125894
Subject Item
_:vb7705638
rdf:type
n2:Context
rdf:value
Consequently, efficient coupling of growth factor signaling to Gαi-dependent Akt enhancement and actin remodeling occurs in GIV-wt cells but not in GIV-FA cells (Garcia-Marcos et al., >>2009<<). Where on the receptor tail GIV binds and which phosphorylation events regulate this interaction remain unknown. Given that a variety of growth factors (VEGF, insulin, and IGF1) (Enomoto et al., 2006) trigger cell migration via GIV, it
n2:mentions
n3:19211784
Subject Item
_:vb7705639
rdf:type
n2:Context
rdf:value
Given that a variety of growth factors (VEGF, insulin, and IGF1) (Enomoto et al., >>2006<<) trigger cell migration via GIV, it is possible that their receptors share a common mechanism.
n2:mentions
n3:17185515
Subject Item
_:vb7705640
rdf:type
n2:Context
rdf:value
This is in keeping with a previous report that EGFR autophosphorylation is essential for motility but not for mitosis (Chen et al., 1994a).
n2:mentions
n3:8106552
Subject Item
_:vb7705641
rdf:type
n2:Context
rdf:value
These differences in receptor localization and contrasting profiles of EGFR-initiated signals we observe in GIV-wt versus GIV-FA cells are in keeping with previous reports (Rijken et al., >>1991<<; Haugh, 2002; Howlin et al., 2008; Iyer et al., 2008) that motogenic signals are initiated and coupled to actin remodeling exclusively by receptors at the PM to preferentially trigger motility, whereas internalized receptors
n2:mentions
n3:1808202
Subject Item
_:vb7705642
rdf:type
n2:Context
rdf:value
These differences in receptor localization and contrasting profiles of EGFR-initiated signals we observe in GIV-wt versus GIV-FA cells are in keeping with previous reports (Rijken et al., 1991; Haugh, >>2002<<; Howlin et al., 2008; Iyer et al., 2008) that motogenic signals are initiated and coupled to actin remodeling exclusively by receptors at the PM to preferentially trigger motility, whereas internalized receptors preferentially propagate
n2:mentions
n3:14993384
Subject Item
_:vb7705643
rdf:type
n2:Context
rdf:value
These differences in receptor localization and contrasting profiles of EGFR-initiated signals we observe in GIV-wt versus GIV-FA cells are in keeping with previous reports (Rijken et al., 1991; Haugh, 2002; Howlin et al., >>2008<<; Iyer et al., 2008) that motogenic signals are initiated and coupled to actin remodeling exclusively by receptors at the PM to preferentially trigger motility, whereas internalized receptors preferentially propagate mitogenic signals,
n2:mentions
n3:18435854
Subject Item
_:vb7705644
rdf:type
n2:Context
rdf:value
differences in receptor localization and contrasting profiles of EGFR-initiated signals we observe in GIV-wt versus GIV-FA cells are in keeping with previous reports (Rijken et al., 1991; Haugh, 2002; Howlin et al., 2008; Iyer et al., >>2008<<) that motogenic signals are initiated and coupled to actin remodeling exclusively by receptors at the PM to preferentially trigger motility, whereas internalized receptors preferentially propagate mitogenic signals, presumably from
n2:mentions
n3:17708541
Subject Item
_:vb7705645
rdf:type
n2:Context
rdf:value
are initiated and coupled to actin remodeling exclusively by receptors at the PM to preferentially trigger motility, whereas internalized receptors preferentially propagate mitogenic signals, presumably from endosomes (Murphy et al., >>2009<<). These differences in EGFR signaling have been attributed to the levels of phosphatidylinositol-4,5-bisphosphate (PI4,5P2), a critical and common substrate of the two key motogenic enzymes PI3K and PLCγ1, which are enriched at the PM but
n2:mentions
n3:19822761
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have been attributed to the levels of phosphatidylinositol-4,5-bisphosphate (PI4,5P2), a critical and common substrate of the two key motogenic enzymes PI3K and PLCγ1, which are enriched at the PM but depleted at endosomes (Haugh, >>2002<<). We conclude that motogenic PI3K and PLCγ1 signals are enhanced in the presence of an intact GEF motif, probably due to the persistence of activated receptor at the PI4,5P2-enriched PM, and inhibited in the absence of a GEF motif,
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That the rates of receptor degradation are accelerated in GIV-wt and delayed in GIV-FA cells may reflect a function of GIV in sorting and trafficking of EGFR (Simpson et al., >>2005<<), perhaps modulated by differential recruitment of c-Cbl (Figure 2, A, E, and G), the ubiquitin ligase that promotes endolysosomal degradation of EGFR (Levkowitz et al., 1998).
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of GIV in sorting and trafficking of EGFR (Simpson et al., 2005), perhaps modulated by differential recruitment of c-Cbl (Figure 2, A, E, and G), the ubiquitin ligase that promotes endolysosomal degradation of EGFR (Levkowitz et al., >>1998<<).
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The distribution of EGFR in GIV-FA cells (decreased at the PM but increased within endosomes) is strikingly similar to that reported previously in cells overexpressing c-Src (Ware et al., >>1997<<). Moreover, we found that increased Src activity in GIV-FA cells is associated with sustained receptor phosphorylation at Y845, a c-Src substrate site, as well as hyperactivation of ERK1/2.
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Enhanced ERK1/2 activation in spite of reduced Grb2 recruitment could be mediated through Src (Frame, >>2004<<). That highly motile GIV-wt cells restrict ERK activity to low levels is consistent with the computational analysis of proteomic networks of the EGFR pathway (Janes and Lauffenburger, 2006), which predicts that low ERK phosphorylation
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That highly motile GIV-wt cells restrict ERK activity to low levels is consistent with the computational analysis of proteomic networks of the EGFR pathway (Janes and Lauffenburger, >>2006<<), which predicts that low ERK phosphorylation favors high-speed motility.
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like GIV-FA cells in that they inhibit motogenic signals and selectively propagate mitogenic signals in response to EGF and are immotile and proliferate rapidly, features that facilitate early tumor growth (Bernards and Weinberg, >>2002<<). In contrast, in highly invasive cancer cells expression of GIV-fl mRNA and protein is up-regulated, and these cells behave like the GIV-wt HeLa cells in that they migrate efficiently (Howlin et al., 2008) via activation of Gαi (Ghosh et
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In contrast, in highly invasive cancer cells expression of GIV-fl mRNA and protein is up-regulated, and these cells behave like the GIV-wt HeLa cells in that they migrate efficiently (Howlin et al., >>2008<<) via activation of Gαi (Ghosh et al., 2008; Garcia-Marcos et al., 2009) but proliferate more slowly (Lelievre et al., 1998; Howlin et al., 2008) and require GIV for efficient tumor invasion (Jiang et al., 2008).
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n3:18435854
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in highly invasive cancer cells expression of GIV-fl mRNA and protein is up-regulated, and these cells behave like the GIV-wt HeLa cells in that they migrate efficiently (Howlin et al., 2008) via activation of Gαi (Ghosh et al., >>2008<<; Garcia-Marcos et al., 2009) but proliferate more slowly (Lelievre et al., 1998; Howlin et al., 2008) and require GIV for efficient tumor invasion (Jiang et al., 2008).
n2:mentions
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cells expression of GIV-fl mRNA and protein is up-regulated, and these cells behave like the GIV-wt HeLa cells in that they migrate efficiently (Howlin et al., 2008) via activation of Gαi (Ghosh et al., 2008; Garcia-Marcos et al., >>2009<<) but proliferate more slowly (Lelievre et al., 1998; Howlin et al., 2008) and require GIV for efficient tumor invasion (Jiang et al., 2008).
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and these cells behave like the GIV-wt HeLa cells in that they migrate efficiently (Howlin et al., 2008) via activation of Gαi (Ghosh et al., 2008; Garcia-Marcos et al., 2009) but proliferate more slowly (Lelievre et al., >>1998<<; Howlin et al., 2008) and require GIV for efficient tumor invasion (Jiang et al., 2008).
n2:mentions
n3:9543252
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cells behave like the GIV-wt HeLa cells in that they migrate efficiently (Howlin et al., 2008) via activation of Gαi (Ghosh et al., 2008; Garcia-Marcos et al., 2009) but proliferate more slowly (Lelievre et al., 1998; Howlin et al., >>2008<<) and require GIV for efficient tumor invasion (Jiang et al., 2008). These features are known to hinder early tumor growth but are required later for metastatic progression (Bernards and Weinberg, 2002).
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(Howlin et al., 2008) via activation of Gαi (Ghosh et al., 2008; Garcia-Marcos et al., 2009) but proliferate more slowly (Lelievre et al., 1998; Howlin et al., 2008) and require GIV for efficient tumor invasion (Jiang et al., >>2008<<). These features are known to hinder early tumor growth but are required later for metastatic progression (Bernards and Weinberg, 2002).
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These features are known to hinder early tumor growth but are required later for metastatic progression (Bernards and Weinberg, >>2002<<). To the best of our knowledge, this is the first example of a protein that undergoes bipartite dysregulation during oncogenesis: In slow-growing, highly invasive cancer cells constitutive splicing allows translation of GIV-fl and
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These results suggest that extrinsic factors, e.g., differential expression of splicing factors during cancer progression (Stickeler et al., >>1999<<), may restrict GIVΔCT expression to poorly invasive cells.
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With advancing clinical stages, invasive tumors are increasingly made up of cells expressing GIV-fl, which endows cells with an invasive advantage (Jiang et al., >>2008<<). This shift in tumor composition is in keeping with studies demonstrating that phenotypic heterogeneity exists among cells within the same tumor (Giese et al., 1996; Fedotov and Iomin, 2007). Phenotypic heterogeneity has remained a
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n3:18316593
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This shift in tumor composition is in keeping with studies demonstrating that phenotypic heterogeneity exists among cells within the same tumor (Giese et al., >>1996<<; Fedotov and Iomin, 2007).
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This shift in tumor composition is in keeping with studies demonstrating that phenotypic heterogeneity exists among cells within the same tumor (Giese et al., 1996; Fedotov and Iomin, >>2007<<). Phenotypic heterogeneity has remained a challenge in treatment of carcinomas because only the actively proliferating cells are the most vulnerable to chemotherapy, whereas the nonproliferating cells that are actively invading are
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in treatment of carcinomas because only the actively proliferating cells are the most vulnerable to chemotherapy, whereas the nonproliferating cells that are actively invading are resistant to anticancer drugs (Mandel and Rall, >>1969<<). Our findings suggest that alternative splicing of GIV's GEF motif probably contributes to phenotypic heterogeneity and influences early tumor growth as well as late metastatic invasion.
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