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bibo:doi: 10.1038%2Fs41388-019-0756-z
n6:contains: _:vb89802982 _:vb89802961 _:vb89802974 _:vb89802947

Subject Item: _:vb89802947
rdf:type: n6:Section
dc:title: introduction
n6:contains: _:vb89802952 _:vb89802953 _:vb89802954 _:vb89802955 _:vb89802956 _:vb89802957 _:vb89802958 _:vb89802959 _:vb89802948 _:vb89802949 _:vb89802950 _:vb89802951 _:vb89802960

Subject Item: _:vb89802948
rdf:type: n2:Context
rdf:value: Brain metastases (BM) are a devastating complication of cancer in terms of cognitive, physical, and quality of life adverse outcomes (rev in [1, >>2<<]). Among the common subtypes of breast cancer, BM preferentially develop in metastatic patients with HER2 -positive disease and triple-negative breast cancers (TNBC), which lack estrogen receptor (ER), progesterone receptor (PR), and HER2
n2:mentions: n3:25670078

Subject Item: _:vb89802949
rdf:type: n2:Context
rdf:value: subtypes of breast cancer, BM preferentially develop in metastatic patients with HER2 -positive disease and triple-negative breast cancers (TNBC), which lack estrogen receptor (ER), progesterone receptor (PR), and HER2 alterations [>>3<<, 4]. Development of BM predicts poorest survival in TNBC patients and results in death within months of diagnosis [3, 5, 6].
n2:mentions: n3:23012306

Subject Item: _:vb89802950
rdf:type: n2:Context
rdf:value: subtypes of breast cancer, BM preferentially develop in metastatic patients with HER2 -positive disease and triple-negative breast cancers (TNBC), which lack estrogen receptor (ER), progesterone receptor (PR), and HER2 alterations [3, >>4<<]. Development of BM predicts poorest survival in TNBC patients and results in death within months of diagnosis [3, 5, 6].
n2:mentions: n3:21067385

Subject Item: _:vb89802951
rdf:type: n2:Context
rdf:value: Development of BM predicts poorest survival in TNBC patients and results in death within months of diagnosis [>>3<<, 5, 6]. While the increased metastatic potential and subsequent worse prognosis of TNBC has been attributed to the intrinsic genetics of these tumors, a young age at diagnosis predicts worse prognosis for various tumor subtypes, including
n2:mentions: n3:23012306

Subject Item: _:vb89802952
rdf:type: n2:Context
rdf:value: Development of BM predicts poorest survival in TNBC patients and results in death within months of diagnosis [3, >>5<<, 6]. While the increased metastatic potential and subsequent worse prognosis of TNBC has been attributed to the intrinsic genetics of these tumors, a young age at diagnosis predicts worse prognosis for various tumor subtypes, including
n2:mentions: n3:23373998

Subject Item: _:vb89802953
rdf:type: n2:Context
rdf:value: Development of BM predicts poorest survival in TNBC patients and results in death within months of diagnosis [3, 5, >>6<<]. While the increased metastatic potential and subsequent worse prognosis of TNBC has been attributed to the intrinsic genetics of these tumors, a young age at diagnosis predicts worse prognosis for various tumor subtypes, including TNBC
n2:mentions: n3:22607041

Subject Item: _:vb89802954
rdf:type: n2:Context
rdf:value: potential and subsequent worse prognosis of TNBC has been attributed to the intrinsic genetics of these tumors, a young age at diagnosis predicts worse prognosis for various tumor subtypes, including TNBC and the luminal B subtype [>>7<<–11]. Young pre-menopausal women with TNBC showed increased incidence of BM (53%) compared to post-menopausal women (28%) [12].
n2:mentions: n3:19460581 n3:18612148 n3:16826579 n3:16931954

Subject Item: _:vb89802955
rdf:type: n2:Context
rdf:value: Young pre-menopausal women with TNBC showed increased incidence of BM (53%) compared to post-menopausal women (28%) [>>12<<]. These data suggested the novel hypothesis that pre-menopausal hormones such as estradiol (E2) may promote BM of TNBC by exerting effects on the brain microenvironment.
n2:mentions: n3:24586742

Subject Item: _:vb89802956
rdf:type: n2:Context
rdf:value: E2 plays pleiotropic roles in brain function through activation of ERs expressed in glial and neuronal cells [>>13<<–15]. Prior studies showed that reactive astrocytes, which surround and infiltrate human and experimental BM, expressed both ER genes (ERα and ERβ) and upregulated epidermal growth factor receptor (EGFR) ligands in response to E2,
n2:mentions: n3:19207814 n3:18195084 n3:21143654

Subject Item: _:vb89802957
rdf:type: n2:Context
rdf:value: human and experimental BM, expressed both ER genes (ERα and ERβ) and upregulated epidermal growth factor receptor (EGFR) ligands in response to E2, promoting migration, invasion, and proliferation of EGFR+ brain-tropic 231BR TNBC cells [>>16<<]. However, 40% of TNBC do not overexpress EGFR [17, 18], raising the possibility that alternative mechanisms contribute to E2 promotion of BM in TNBC.
n2:mentions: n3:26411365

Subject Item: _:vb89802958
rdf:type: n2:Context
rdf:value: However, 40% of TNBC do not overexpress EGFR [>>17<<, 18], raising the possibility that alternative mechanisms contribute to E2 promotion of BM in TNBC.
n2:mentions: n3:21424932

Subject Item: _:vb89802959
rdf:type: n2:Context
rdf:value: However, 40% of TNBC do not overexpress EGFR [17, >>18<<], raising the possibility that alternative mechanisms contribute to E2 promotion of BM in TNBC.
n2:mentions: n3:18980022

Subject Item: _:vb89802960
rdf:type: n2:Context
rdf:value: TrkB has been shown to mark a subpopulation of putative cancer stem cells in recurrent TNBC, promote anoikis-resistance, and increase metastatic potential [>>19<<–23]. We show that E2-upregulated BDNF in ER+ astrocytes and cancer cells activated TrkB signaling and increased the invasiveness and tumor-initiating capacity of TNBC cells in vitro. Moreover, BDNF cross-activated TrkB and EGFR in cancer
n2:mentions: n3:23185507 n3:24531713 n3:24982195 n3:26515594 n3:15329723

Subject Item: _:vb89802961
rdf:type: n6:Section
dc:title: results
n6:contains: _:vb89802962 _:vb89802963 _:vb89802964 _:vb89802965 _:vb89802966 _:vb89802967 _:vb89802968 _:vb89802969 _:vb89802970 _:vb89802971 _:vb89802972 _:vb89802973

Subject Item: _:vb89802962
rdf:type: n2:Context
rdf:value: Prior studies showed that E2 promotes brain metastatic colonization of a brain-tropic subline of human TN MDA-MB-231 breast cancer cells (231BR) [>>24<<] via paracrine activation of EGFR [16]. These cells express higher levels of EGFR compared to other TNBC cell lines (4T1BR5, E0771, F2-7, Fig.
n2:mentions: n3:11499871

Subject Item: _:vb89802963
rdf:type: n2:Context
rdf:value: Prior studies showed that E2 promotes brain metastatic colonization of a brain-tropic subline of human TN MDA-MB-231 breast cancer cells (231BR) [24] via paracrine activation of EGFR [>>16<<]. These cells express higher levels of EGFR compared to other TNBC cell lines (4T1BR5, E0771, F2-7, Fig.
n2:mentions: n3:26411365

Subject Item: _:vb89802964
rdf:type: n2:Context
rdf:value: BM were quantified histologically as previously described [>>25<<], or ex-vivo imaging of brains at euthanasia (for E0771-GFP-luc) was performed.
n2:mentions: n3:17483330

Subject Item: _:vb89802965
rdf:type: n2:Context
rdf:value: Cancer cells seeded on top of brain slices from E2-treated mice showed increased number of invading branches (measured using Sholl analysis) [>>26<<] compared to cancer cells seeded on top of slices from OVX-treated mice (Fig.
n2:mentions: n3:25264773

Subject Item: _:vb89802966
rdf:type: n2:Context
rdf:value: As these TNBC cells lack ERα and are unresponsive to direct effects of E2 [>>16<<] (Supplementary Fig.
n2:mentions: n3:26411365

Subject Item: _:vb89802967
rdf:type: n2:Context
rdf:value: We reported that ER+ astrocytes surround experimental 231BR and human BM [>>16<<]. Double immunofluorescence (IF) demonstrated that astrocytes surrounding 4T1BR5 BM expressed membrane and nuclear ERα (Fig.
n2:mentions: n3:26411365

Subject Item: _:vb89802968
rdf:type: n2:Context
rdf:value: Since there are a limited number of models of TNBC-BM, we derived a novel TNBC cell line (F2-7) from a BM-PDX [>>27<<]. Full length TrkB (possessing an intracellular kinase domain) in its glycosylated and unglycosylated forms (~140 and 110 kD) [28, 29] was detected in all brain-trophic cell lines from human (231BR, F2-7) and murine (4T1BR5, E0771) origin
n2:mentions: n3:29164052

Subject Item: _:vb89802969
rdf:type: n2:Context
rdf:value: Full length TrkB (possessing an intracellular kinase domain) in its glycosylated and unglycosylated forms (~140 and 110 kD) [>>28<<, 29] was detected in all brain-trophic cell lines from human (231BR, F2-7) and murine (4T1BR5, E0771) origin (Fig.
n2:mentions: n3:1846020

Subject Item: _:vb89802970
rdf:type: n2:Context
rdf:value: Full length TrkB (possessing an intracellular kinase domain) in its glycosylated and unglycosylated forms (~140 and 110 kD) [28, >>29<<] was detected in all brain-trophic cell lines from human (231BR, F2-7) and murine (4T1BR5, E0771) origin (Fig.
n2:mentions: n3:14603320

Subject Item: _:vb89802971
rdf:type: n2:Context
rdf:value: Activation of TrkB promotes migration of neurons and invasion of cancer cells [>>30<<, 31], thus we investigated if BDNF/TrkB activation promoted invasion in TNBC cells.
n2:mentions: n3:20173744

Subject Item: _:vb89802972
rdf:type: n2:Context
rdf:value: Activation of TrkB promotes migration of neurons and invasion of cancer cells [30, >>31<<], thus we investigated if BDNF/TrkB activation promoted invasion in TNBC cells.
n2:mentions: n3:24959744

Subject Item: _:vb89802973
rdf:type: n2:Context
rdf:value: Given that E2-treated astrocytes activate both EGFR [>>16<<] and TrkB ligands on brain metastatic cancer cells and the majority of human BM are EGFR+, we assessed how EGFR and TrkB activation contributed to signaling and metastatic traits in EGFR+TrkB+ TNBC cells.
n2:mentions: n3:26411365

Subject Item: _:vb89802974
rdf:type: n6:Section
dc:title: methods
n6:contains: _:vb89802980 _:vb89802981 _:vb89802976 _:vb89802977 _:vb89802978 _:vb89802979 _:vb89802975

Subject Item: _:vb89802975
rdf:type: n2:Context
rdf:value: Suyun Huang) were maintained as described [>>24<<, 27, 62]. E0771 cells were purchased from CH3 BioSystems, LLC (Buffalo, NY) and maintained in RPMI supplemented with 5% FBS.
n2:mentions: n3:11499871

Subject Item: _:vb89802976
rdf:type: n2:Context
rdf:value: Suyun Huang) were maintained as described [24, >>27<<, 62]. E0771 cells were purchased from CH3 BioSystems, LLC (Buffalo, NY) and maintained in RPMI supplemented with 5% FBS.
n2:mentions: n3:29164052

Subject Item: _:vb89802977
rdf:type: n2:Context
rdf:value: Suyun Huang) were maintained as described [24, 27, >>62<<]. E0771 cells were purchased from CH3 BioSystems, LLC (Buffalo, NY) and maintained in RPMI supplemented with 5% FBS.
n2:mentions: n3:20829328

Subject Item: _:vb89802978
rdf:type: n2:Context
rdf:value: Primary astrocytes were cultured as described [>>63<<]. To obtain 10× concentrated astrocytic-conditioned media (CM), 100% confluent astrocyte cultures were incubated for 72 h with serum-free phenol-red free media containing vehicle (CM-OH) or 10 nM E2 (CM-E2).
n2:mentions: n3:22144299

Subject Item: _:vb89802979
rdf:type: n2:Context
rdf:value: Images were exported to ImageJ software (NIH) and spread of GFP+ cells (green mask) away from the edge of the mammosphere were quantified using Sholl analysis [>>26<<].
n2:mentions: n3:25264773

Subject Item: _:vb89802980
rdf:type: n2:Context
rdf:value: Letrozole, an aromatase inhibitor known to cross the BBB [>>64<<], was diluted in 0.3% hydroxyl-propyl cellulose at 0.2 mg/ml and injected subcutaneously (10 µg/day).
n2:mentions: n3:20097718

Subject Item: _:vb89802981
rdf:type: n2:Context
rdf:value: ROIs were made using Confocal Uniovi 1–51 an ImageJ bundle [>>65<<]. Minor linear adjustments to brightness and contrast were performed identically and in parallel.
n2:mentions: n3:22930834

Subject Item: _:vb89802982
rdf:type: n6:Section
dc:title: discussion
n6:contains: _:vb89802996 _:vb89802997 _:vb89802998 _:vb89802999 _:vb89802992 _:vb89802993 _:vb89802994 _:vb89802995 _:vb89802988 _:vb89802989 _:vb89802990 _:vb89802991 _:vb89802984 _:vb89802985 _:vb89802986 _:vb89802987 _:vb89802983

Subject Item: _:vb89802983
rdf:type: n2:Context
rdf:value: Consistent with the known role of E2 in modulating neuroinflammatory responses in the brain via activation of ERs in glial cells [>>32<<, 33], ERα was expressed in reactive astrocytes at early and late stages of BMs in the 4T1BR5 model.
n2:mentions: n3:20881113

Subject Item: _:vb89802984
rdf:type: n2:Context
rdf:value: Consistent with the known role of E2 in modulating neuroinflammatory responses in the brain via activation of ERs in glial cells [32, >>33<<], ERα was expressed in reactive astrocytes at early and late stages of BMs in the 4T1BR5 model.
n2:mentions: n3:21555578

Subject Item: _:vb89802985
rdf:type: n2:Context
rdf:value: Reactive astrocytes surround cancer cells early during brain colonization and are critical for the establishment and growth of BM [>>34<<–40], thus, it is likely that E2 action on ER+ astrocytes influences multiple steps in the brain colonization cascade.
n2:mentions: n3:21390191 n3:27225120 n3:29892069 n3:24581498 n3:20382702 n3:26479035 n3:24324647

Subject Item: _:vb89802986
rdf:type: n2:Context
rdf:value: While quantifying the percentage of ER+ cells in the subset of GFAP+ cells limits the bias introduced by increased number of GFAP+ cells, upregulation of ERs in reactive astrocytes upon brain injury in primates has been reported [>>41<<], raising the possibility that increased ERα results from more BM-associated reactive astrocytes in E2-treated mice.
n2:mentions: n3:11283953

Subject Item: _:vb89802987
rdf:type: n2:Context
rdf:value: BDNF is best known as a neurotrophic factor that promotes survival of neurons and plays critical roles during brain development [>>42<<, 43]. BDNF levels are very low (pg/g) in the unlesioned adult brain [44, 45], but injuries and various signals lead to upregulation and secretion of BDNF by astrocytes [46–48].
n2:mentions: n3:11040419

Subject Item: _:vb89802988
rdf:type: n2:Context
rdf:value: BDNF is best known as a neurotrophic factor that promotes survival of neurons and plays critical roles during brain development [42, >>43<<]. BDNF levels are very low (pg/g) in the unlesioned adult brain [44, 45], but injuries and various signals lead to upregulation and secretion of BDNF by astrocytes [46–48].
n2:mentions: n3:20162032

Subject Item: _:vb89802989
rdf:type: n2:Context
rdf:value: BDNF levels are very low (pg/g) in the unlesioned adult brain [>>44<<, 45], but injuries and various signals lead to upregulation and secretion of BDNF by astrocytes [46–48].
n2:mentions: n3:18204444

Subject Item: _:vb89802990
rdf:type: n2:Context
rdf:value: BDNF levels are very low (pg/g) in the unlesioned adult brain [44, >>45<<], but injuries and various signals lead to upregulation and secretion of BDNF by astrocytes [46–48].
n2:mentions: n3:7188352

Subject Item: _:vb89802991
rdf:type: n2:Context
rdf:value: BDNF levels are very low (pg/g) in the unlesioned adult brain [44, 45], but injuries and various signals lead to upregulation and secretion of BDNF by astrocytes [>>46<<–48]. In this study, E2 upregulated transcription of BDNF leading to increased pro-BDNF and mature BDNF protein levels in astrocytes (Fig. 2a). Secreted pro-BDNF is cleaved to BDNF by the tissue plasminogen activator (tPA)/plasmin protease
n2:mentions: n3:24920623 n3:26468200 n3:11114257

Subject Item: _:vb89802992
rdf:type: n2:Context
rdf:value: Secreted pro-BDNF is cleaved to BDNF by the tissue plasminogen activator (tPA)/plasmin protease system in the brain [>>49<<–51], suggesting that astrocytic BDNF reaches cancer cells within the brain niche as mature BDNF.
n2:mentions: n3:21371535 n3:15494978 n3:15486301

Subject Item: _:vb89802993
rdf:type: n2:Context
rdf:value: E2 has been shown to upregulate BDNF in some neuronal types [>>52<<, 53], thus, it is possible that neurons and other ER+ cells in the brain microenvironment could contribute to the pro-metastatic effects of E2 in the brain niche.
n2:mentions: n3:7479947

Subject Item: _:vb89802994
rdf:type: n2:Context
rdf:value: E2 has been shown to upregulate BDNF in some neuronal types [52, >>53<<], thus, it is possible that neurons and other ER+ cells in the brain microenvironment could contribute to the pro-metastatic effects of E2 in the brain niche.
n2:mentions: n3:10393979

Subject Item: _:vb89802995
rdf:type: n2:Context
rdf:value: autocrine action of BDNF has been demonstrated in neurons, whereby extracellular BDNF triggers BDNF secretion from neurites and promotes surface insertion of TrkB receptor via Pi3K activation, amplifying BDNF/TrkB signaling [>>54<<]. Here, BDNF and E2-treated astrocytes triggered BDNF protein synthesis, and knockdown of TrkB in cancer cells abolished this upregulation, demonstrating the existence of a similar positive feedback loop of BDNF/TrkB in cancer cells.
n2:mentions: n3:22025720

Subject Item: _:vb89802996
rdf:type: n2:Context
rdf:value: BDNF-mediated activation of EGFR has been observed in lung cancer [>>31<<] and suggests BDNF/TrkB/EGFR cross-talk is a more general mechanism promoting BM.
n2:mentions: n3:24959744

Subject Item: _:vb89802997
rdf:type: n2:Context
rdf:value: Recent studies reported a similar convergence between BDNF/TrkB and HER2 in BM [>>55<<], suggesting that E2-upregulated BDNF/TrkB activation may also promote BM in younger women with HER2+ tumors.
n2:mentions: n3:28446206

Subject Item: _:vb89802998
rdf:type: n2:Context
rdf:value: This is consistent with prior reports showing that E2 can promote tumor growth and metastasis via mobilization of myeloid-derived suppressor cells [>>56<<–58]. Thus, E2-depletion therapies may benefit overall survival in younger women with TNBC by decreasing both brain and systemic metastasis. The extent to which ovarian E2 depletion alone decreased metastasis varied among cell lines, as
n2:mentions: n3:22523036 n3:22467173 n3:27694385

Subject Item: _:vb89802999
rdf:type: n2:Context
rdf:value: Since OVX mice still died, it is possible that brain micrometastasis observed in OVX mice can progress in the presence of brain-synthesized estrogens [>>59<<–61]. Additionally, 4T1BR5 cells are not labeled, thus, it cannot be discounted that some extracranial metastasis affect survival. Given that full estrogen depletion (OVX + Letrozole) was more effective in decreasing BM in the E0771 model,
n2:mentions: n3:25698781 n3:21320576

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