We are analyzing https://link.springer.com/article/10.1186/s12964-019-0367-x.

Title:
Estrogen receptor α-NOTCH1 axis enhances basal stem-like cells and epithelial-mesenchymal transition phenotypes in prostate cancer | Cell Communication and Signaling
Description:
Background Prostate cancer (PCa) is the second leading cause of mortality and a leading cause of malignant tumors in males. Prostate cancer stem cells (PCSCs) are likely the responsible cell types for cancer initiation, clinical treatment failure, tumor relapse, and metastasis. Estrogen receptor alpha (ERα) is mainly expressed in the basal layer cells of the normal prostate gland and has key roles in coordinating stem cells to control prostate organ development. Here, we investigated the roles of the estrogen-ERα signaling pathway in regulating PCSCs. Methods Correlation of CD49f and ERα/NOTCH1 was analyzed in human clinical datasets and tissue samples. Flow cytometry was used to sort CD49fHi and CD49fLow cells. EZH2 recruitment by ERα and facilitation of ERα binding to the NOTCH1 promoter was validated by Co-IP and ChIP. Primary tumor growth, tumor metastasis and sensitivity to 17β-estradiol (E2) inhibitor (tamoxifen) were evaluated in castrated mice. Results ERα expression was significantly higher in CD49fHi prostate cancer basal stem-like cells (PCBSLCs), which showed basal and EMT features with susceptibility to E2 treatment. ERα-induced estrogen effects were suggested to drive the NOTCH1 signaling pathway activity via binding to the NOTCH1 promoter. Moreover, EZH2 was recruited by ERα and acted as a cofactor to assist ERα-induced estrogen effects in regulating NOTCH1 in PCa. In vivo, E2 promoted tumor formation and metastasis, which were inhibited by tamoxifen. Conclusions Our results implicated CD49f+/ERα + prostate cancer cells associated with basal stem-like and EMT features, named EMT-PCBSLCs, in heightened potential for promoting metastasis. NOTCH1 was regulated by E2 in CD49fHi EMT-PCBSLCs. These results contribute to insights into the metastatic mechanisms of EMT-PCBSLCs in PCa.
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Keywords {🔍}

cells, notch, prostate, cancer, expression, erα, cell, lncapabl, cdf, stem, analysis, article, google, scholar, fig, estrogen, basal, results, pca, cas, emt, showed, ezh, data, metastasis, cdfhi, pcscs, tamoxifen, tumors, promoter, additional, signaling, normal, file, treated, tcga, tissues, treatment, samples, prad, tumor, chip, primary, breast, markers, pcbslcs, luminal, zhang, higher, erαinduced,

Topics {✒️}

ice-cold phosphate-buffered saline epithelial-mesenchymal transition phenotypes er-positive breast cancer estrogen receptor–regulated transcription estrogen receptor-α estrogen receptor α erα-induced estrogen effects estrogen receptor alpha injected lncap-abl-green cells castration-resistant prostate cancer tumor-initiating cell activities cancer stem cells--perspectives cd49f+/erα + prostate cancer cells 5 × sds-page loading buffer ras/mapk activation cooperate estrogen-erα signaling pathway luminal cell-fate commitment estrogen receptor-beta expression national cancer center ar-positive lncap-abl cells tamoxifen-resistant breast cancer androgen-independent prostate cancer low-expressing cells showed article download pdf 100 mg/ml penicillin/streptomycin lncap-abl cell lines notch1 double-positive cells increase cd49f-positive cells epithelial-mesenchymal transition lncap-abl stem cells cancer genome atlas estrogen enhanced cscs estrogen receptor-β western blot results showed named lncap-abl-green vimentin double-positive cells estrogen signaling pathway cd49f+/erα+ expressing cells 1 × 106 lncap-abl-green cells lncap-abl-green cells higher-gleason stage carcinomas mammary tumor regression estrogen receptor expression privacy choices/manage cookies lncap-abl cells showed cold spring harbor ��ct reference-∆ct target human prostate cancer prostatic neoplasms induced ar-negative pc3 cells

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         description:Prostate cancer (PCa) is the second leading cause of mortality and a leading cause of malignant tumors in males. Prostate cancer stem cells (PCSCs) are likely the responsible cell types for cancer initiation, clinical treatment failure, tumor relapse, and metastasis. Estrogen receptor alpha (ERα) is mainly expressed in the basal layer cells of the normal prostate gland and has key roles in coordinating stem cells to control prostate organ development. Here, we investigated the roles of the estrogen-ERα signaling pathway in regulating PCSCs. Correlation of CD49f and ERα/NOTCH1 was analyzed in human clinical datasets and tissue samples. Flow cytometry was used to sort CD49fHi and CD49fLow cells. EZH2 recruitment by ERα and facilitation of ERα binding to the NOTCH1 promoter was validated by Co-IP and ChIP. Primary tumor growth, tumor metastasis and sensitivity to 17β-estradiol (E2) inhibitor (tamoxifen) were evaluated in castrated mice. ERα expression was significantly higher in CD49fHi prostate cancer basal stem-like cells (PCBSLCs), which showed basal and EMT features with susceptibility to E2 treatment. ERα-induced estrogen effects were suggested to drive the NOTCH1 signaling pathway activity via binding to the NOTCH1 promoter. Moreover, EZH2 was recruited by ERα and acted as a cofactor to assist ERα-induced estrogen effects in regulating NOTCH1 in PCa. In vivo, E2 promoted tumor formation and metastasis, which were inhibited by tamoxifen. Our results implicated CD49f+/ERα + prostate cancer cells associated with basal stem-like and EMT features, named EMT-PCBSLCs, in heightened potential for promoting metastasis. NOTCH1 was regulated by E2 in CD49fHi EMT-PCBSLCs. These results contribute to insights into the metastatic mechanisms of EMT-PCBSLCs in PCa.
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      description:Prostate cancer (PCa) is the second leading cause of mortality and a leading cause of malignant tumors in males. Prostate cancer stem cells (PCSCs) are likely the responsible cell types for cancer initiation, clinical treatment failure, tumor relapse, and metastasis. Estrogen receptor alpha (ERα) is mainly expressed in the basal layer cells of the normal prostate gland and has key roles in coordinating stem cells to control prostate organ development. Here, we investigated the roles of the estrogen-ERα signaling pathway in regulating PCSCs. Correlation of CD49f and ERα/NOTCH1 was analyzed in human clinical datasets and tissue samples. Flow cytometry was used to sort CD49fHi and CD49fLow cells. EZH2 recruitment by ERα and facilitation of ERα binding to the NOTCH1 promoter was validated by Co-IP and ChIP. Primary tumor growth, tumor metastasis and sensitivity to 17β-estradiol (E2) inhibitor (tamoxifen) were evaluated in castrated mice. ERα expression was significantly higher in CD49fHi prostate cancer basal stem-like cells (PCBSLCs), which showed basal and EMT features with susceptibility to E2 treatment. ERα-induced estrogen effects were suggested to drive the NOTCH1 signaling pathway activity via binding to the NOTCH1 promoter. Moreover, EZH2 was recruited by ERα and acted as a cofactor to assist ERα-induced estrogen effects in regulating NOTCH1 in PCa. In vivo, E2 promoted tumor formation and metastasis, which were inhibited by tamoxifen. Our results implicated CD49f+/ERα + prostate cancer cells associated with basal stem-like and EMT features, named EMT-PCBSLCs, in heightened potential for promoting metastasis. NOTCH1 was regulated by E2 in CD49fHi EMT-PCBSLCs. These results contribute to insights into the metastatic mechanisms of EMT-PCBSLCs in PCa.
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         Cytokines and Growth Factors
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