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n4:pmcid: PMC0
bibo:doi: 10.1371%2Fjournal.pone.0037960
n5:contains: _:vb16320664 _:vb16320678 _:vb16320686 _:vb16320681

Subject Item: _:vb16320664
rdf:type: n5:Section
dc:title: introduction
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Subject Item: _:vb16320665
rdf:type: n4:Context
rdf:value: The bond of cell surface receptors with ligands, such as interleukin-6 (IL-6) or epidermal growth factor (EGFR), induces tyrosine phosphorylation of STAT3 protein by Janus kinase and growth factor receptor tyrosine kinases [>>1<<]. The activated dimeric form of phospho- STAT3 translocates to the nucleus and regulates the expression of genes containing STAT3-binding sites in their promoters [2]. The activation of STAT3 protein is rapid and transient in normal cells.
n4:mentions: n2:19962667

Subject Item: _:vb16320666
rdf:type: n4:Context
rdf:value: The activated dimeric form of phospho- STAT3 translocates to the nucleus and regulates the expression of genes containing STAT3-binding sites in their promoters [>>2<<]. The activation of STAT3 protein is rapid and transient in normal cells. STAT3 regulates fundamental biological processes,including cell proliferation, survival, and development. Recently, accumulating evidence indicates that
n4:mentions: n2:17332277

Subject Item: _:vb16320667
rdf:type: n4:Context
rdf:value: Recently, accumulating evidence indicates that abnormalities in the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway are involved in the oncogenesis of several cancers [>>3<<].
n4:mentions: n2:19047094

Subject Item: _:vb16320668
rdf:type: n4:Context
rdf:value: Activated STAT3 (nuclear pSTAT3) is expressed in about 55% of NSCLC tumors, as measured by immunohistochemical analyses[>>4<<]–[6]. STAT3 activation is observed in the majority of NSCLC cell lines [7], [8]. In contrast to NSCLC, strong pSTAT3 expression was demonstrated in 100% (10/10) of SCLC tumor tissues tested [9].
n4:mentions: n2:18060032

Subject Item: _:vb16320669
rdf:type: n4:Context
rdf:value: Activated STAT3 (nuclear pSTAT3) is expressed in about 55% of NSCLC tumors, as measured by immunohistochemical analyses[4]–[>>6<<]. STAT3 activation is observed in the majority of NSCLC cell lines [7], [8]. In contrast to NSCLC, strong pSTAT3 expression was demonstrated in 100% (10/10) of SCLC tumor tissues tested [9].
n4:mentions: n2:16959370

Subject Item: _:vb16320670
rdf:type: n4:Context
rdf:value: STAT3 activation is observed in the majority of NSCLC cell lines [>>7<<], [8]. In contrast to NSCLC, strong pSTAT3 expression was demonstrated in 100% (10/10) of SCLC tumor tissues tested [9].
n4:mentions: n2:16203784

Subject Item: _:vb16320671
rdf:type: n4:Context
rdf:value: STAT3 activation is observed in the majority of NSCLC cell lines [7], [>>8<<]. In contrast to NSCLC, strong pSTAT3 expression was demonstrated in 100% (10/10) of SCLC tumor tissues tested [9].
n4:mentions: n2:12833138

Subject Item: _:vb16320672
rdf:type: n4:Context
rdf:value: In contrast to NSCLC, strong pSTAT3 expression was demonstrated in 100% (10/10) of SCLC tumor tissues tested [>>9<<]. However, the mechanism by which dysregulated STAT3 signaling contributes to the progression of human small cell lung cancer (SCLC) has not been elucidated. SCLC is known to have a more aggressive biology with rapid growth and early
n4:mentions: n2:19455144

Subject Item: _:vb16320673
rdf:type: n4:Context
rdf:value: SCLC is known to have a more aggressive biology with rapid growth and early spread, as well as a common association with paraneoplastic syndromes [>>10<<]. Of all histologic types of lung cancer, SCLC is the most sensitive to chemotherapy and radiation, but prognosis remains poor, with an overall median survival following treatment of 10 months and a 5-year survival of 5% [11]. Elderly lung
n4:mentions: n2:10841143

Subject Item: _:vb16320674
rdf:type: n4:Context
rdf:value: It is safe and nontoxic and has demonstrable antitumor, antiinflammatory, apoptotic, and antioxidant properties [>>13<<]. Especially for its anticarcinogenic property, still has been the subject of a great deal of interest. Increasing evidence indicated that curcumin has anticancer effects against different types of human tumor cells, including of ovarian
n4:mentions: n2:16018877

Subject Item: _:vb16320675
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rdf:value: Increasing evidence indicated that curcumin has anticancer effects against different types of human tumor cells, including of ovarian cancer cells, colon cancer cells and astroglioma cells [>>14<<], [15]. This anticancer effects of curcumin were identified through interfering with the cell cycle, inducing apoptosis, and inhibiting the invasive potential of cancers. However, the underlying mechanisms of this anticancer effects are
n4:mentions: n2:15488631

Subject Item: _:vb16320676
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rdf:value: Increasing evidence indicated that curcumin has anticancer effects against different types of human tumor cells, including of ovarian cancer cells, colon cancer cells and astroglioma cells [14], [>>15<<]. This anticancer effects of curcumin were identified through interfering with the cell cycle, inducing apoptosis, and inhibiting the invasive potential of cancers. However, the underlying mechanisms of this anticancer effects are still
n4:mentions: n2:14597785

Subject Item: _:vb16320677
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rdf:value: We have shown previously that curcumin inhibits SCLC cell growth and induces SCLC cell apoptosis [>>16<<]. In the present study, we investigated the molecular mechanisms by which curcumin suppress migration and invasion in SCLC cells. Our aim was to determine the role of JAK/STAT signaling in SCLC progression and test the hypothesis that
n4:mentions: n2:21711158

Subject Item: _:vb16320678
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dc:title: materials and methods
n5:contains: _:vb16320680 _:vb16320679

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rdf:value: NCI-H446 and NCI-1688 (human SCLC) cell lines from our previous published paper [>>15<<] were cultured in RPMI-1640 supplemented with 10% HyClone fetal bovine serum (FBS) (ThermoFisher Scientific, Fremont, CA, USA) in an atmosphere of 5% CO2 at 37°C.
n4:mentions: n2:14597785

Subject Item: _:vb16320680
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rdf:value: The cancer cell transwell migration assay was performed according to previous study and partially modified [>>34<<]. Briefly, Transwell membrane (Corning Costar Corporation) was used. The SCLC cells were trypsinized, washed, and kept suspended in medium without FBS.
n4:mentions: n2:14722241

Subject Item: _:vb16320681
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dc:title: results
n5:contains: _:vb16320682 _:vb16320683 _:vb16320684 _:vb16320685

Subject Item: _:vb16320682
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rdf:value: To reconfirm previous reports [>>17<<], [18] that IL-6 induces proliferation of cancer cells, we serum-starved NCI-H446 and NCI-1688 cells for 12 h and then cultured them in the absence or presence of different concentrations of IL-6 for 24 h, 48 h and 72 h.
n4:mentions: n2:19118018

Subject Item: _:vb16320683
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rdf:value: The half maximal inhibitory concentration (IC50) value of curcumin was 15 µM in SCLC cells from our previous published paper [>>16<<]. Therefore, at 25 ng/ml concentration IL-6 and 15 µM concentration curcumin were used in the following experiment. SiSTAT3 alone or 15 µM curcumin had significant effect on cell proliferation, compared with control cells (Fig. 3).
n4:mentions: n2:21711158

Subject Item: _:vb16320684
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rdf:value: The anchorage-independent growth of SCLC cells was determined in a soft agar assay [>>19<<]. NCI-H446 cells were able to build large aggregates in the soft agar during the 15 days observation period. In contrast, there was no proliferation in the presence of siSTAT3 or curcumin, which suggests a contribution for this pathway in
n4:mentions: n2:9560282

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rdf:value: JAK-2 is a recognized activator of STAT3 [>>20<<]. We investigated whether the inhibitory effects of curcumin on the activation of STAT were due to the suppression of JAK expression in SCLC cells.
n4:mentions: n2:9287210

Subject Item: _:vb16320686
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dc:title: discussion
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Subject Item: _:vb16320687
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rdf:value: Cyclin B1, which is overexpressed in a variety of tumors, is regulated by STAT3 and is required for cells to advance from the G2 phase to the M phase of the cell cycle [>>22<<], [23]. This finding demonstrates for the first time that curcumin has an arrest effect on cell cycle progression involving the G2/M phase in SCLC cells. It also may explain the antiproliferative effects of curcumin. Our laboratory has
n4:mentions: n2:12483537

Subject Item: _:vb16320688
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rdf:value: Cyclin B1, which is overexpressed in a variety of tumors, is regulated by STAT3 and is required for cells to advance from the G2 phase to the M phase of the cell cycle [22], [>>23<<]. This finding demonstrates for the first time that curcumin has an arrest effect on cell cycle progression involving the G2/M phase in SCLC cells. It also may explain the antiproliferative effects of curcumin. Our laboratory has shown
n4:mentions: n2:10783304

Subject Item: _:vb16320689
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rdf:value: processes, and its overexpression by malignant cells has been shown to enhance cellular invasion, induce angiogenesis, regulate antiapoptotic cellular defenses, and augment immunologic resistance through production of prostaglandin E2 [>>25<<]. MMP-2 and MMP-9 plays a crucial role in tumor invasion and angiogenesis by mediating degradation of the extracellular matrix, and inhibition of MMP activity has been shown to suppress lung cancer metastasis [26].
n4:mentions: n2:12384564

Subject Item: _:vb16320690
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rdf:value: MMP-2 and MMP-9 plays a crucial role in tumor invasion and angiogenesis by mediating degradation of the extracellular matrix, and inhibition of MMP activity has been shown to suppress lung cancer metastasis [>>26<<].
n4:mentions: n2:12040437

Subject Item: _:vb16320691
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rdf:value: These results are in accordance with studies by Saydmohammed et al [>>27<<]. They found that curcumin failed to inhibit the phosphorylation of STAT3 at Ser727 in endometrial and ovarian cancer cells.
n4:mentions: n2:20235152

Subject Item: _:vb16320692
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rdf:value: In many tumors and cancer cells, constitutive activation of STAT3 is IL-6 dependent, through either autocrine or paracrine signaling, which seems to be widely expressed in cancer cell lines [>>28<<]. In some cases, the activation of the STAT3 pathway is correlated with brisk intratumoral inflammatory cells infiltration, which means that STAT3 activation may be via paracrine mechanisms [29].
n4:mentions: n2:19457231

Subject Item: _:vb16320693
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rdf:value: In some cases, the activation of the STAT3 pathway is correlated with brisk intratumoral inflammatory cells infiltration, which means that STAT3 activation may be via paracrine mechanisms [>>29<<]. As to this case, inhibition of STAT3 caused decreased production of IL-6.The activation of STAT3 pathway has been studied in patients’ tumor tissue samples. The levels of p-STAT3 expression correlated with the survival rate and severity
n4:mentions: n2:19762335

Subject Item: _:vb16320694
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rdf:value: These results suggested that STAT3 may not only serve as a predictive marker of drug resistance, but also as a prognosis marker of tumors [>>32<<].
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