We are analyzing https://link.springer.com/article/10.1186/1476-4598-8-111.

Title:
Dual effects of TGF-β on ERα-mediated estrogenic transcriptional activity in breast cancer | Molecular Cancer
Description:
Background TGF-β resistance often develops in breast cancer cells that in turn overproduce this cytokine to create a local immunosuppressive environment that fosters tumor growth and exacerbates the invasive and metastatic behavior of the tumor cells themselves. Smads-mediated cross-talk with the estrogen receptor has been implied to play an important role in development and/or progression of breast cancer. We investigated how TGF-β regulates ERα-induced gene transcription and potential mechanisms of frequent TGF-β resistance in breast cancer. Methods Effect of TGF-β on ERα-mediated gene transcription was investigated in breast cancer cell lines using transient transfection, real-time PCR, sequential DNA precipitation, and small interfering RNA assays. The expression of Smads on both human breast cancer cell lines and ERα-positive human breast cancer tissue was evaluated by immunofluorescence and immunohistochemical assays. Results A complex of Smad3/4 mediates TGF-β inhibition of ERα-mediated estrogenic activity of gene transcription in breast cancer cells, and Smad4 is essential and sufficient for such repression. Either overexpression of Smad3 or inhibition of Smad4 leads to the "switch" of TGF-β from a repressor to an activator. Down-regulation and abnormal cellular distribution of Smad4 were associated with some ERα-positive infiltrating human breast carcinoma. There appears a dynamic change of Smad4 expression from benign breast ductal tissue to infiltrating ductal carcinoma. Conclusion These results suggest that aberrant expression of Smad4 or disruption of Smad4 activity lead to the loss of TGF-β suppression of ERα transactivity in breast cancer cells.
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Keywords {🔍}

smad, breast, tgfβ, cancer, cells, expression, erα, pubmed, article, google, scholar, cell, cas, transcription, carcinoma, human, signaling, growth, estrogen, figure, activity, mcf, infiltrating, protein, erαpositive, transcriptional, gene, inhibition, ductal, genes, receptor, complex, role, treated, tumor, mdamb, data, erαmediated, tissue, nucleus, shown, dna, results, transforming, cmyc, sirna, lines, benign, target, assay,

Topics {✒️}

transforming growth factor-beta transforming growth factor-β anti-estrogen-dependent growth inhibition estrogen-induced gene transcription tgf-β-treated mda-mb-231 cells tgf-beta induces assembly erα-positive breast carcinoma erα-mediated gene transcription open access article signet-ring cell carcinoma inhibit erα-induced transcription erα-mediated estrogenic activity article download pdf reconstituted erα-mediated signaling xu cao & mei wan regulates gene transcription β-actin upper primer β-actin lower primer tgf-β stimulated translocation stimulated estrogen-induced ps2 full size image dual-luciferase™ assay kit tgf-β growth inhibition phosphorylated r-smad associates tgf-β stimulation contributes tgf-β signaling pathway mediate tgf-β suppression tgf-β-mediated repression tgf-β-mediated inhibition tgf-β signaling components serial paraffin-embedded sections activate er-target genes estrogen response element intact tgf-β/smad tgf-β-induced phosphorylation infiltrating ductal carcinoma biotin-labeled wild-type erα-mediated transcriptional activation acute myelogenous leukemia elevated tgf-β expression frequent tgf-β resistance tgf-β responsive genes real-time pcr endogenous β-actin mrna erα-induced transcription c-myc upper primer c-myc lower primer human breast tissue human breast carcinoma estrogen-responsive element

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Lindstrom MS, Zhang Y: B23 and ARF: friends or foes?

Schema {🗺️}

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         description:TGF-β resistance often develops in breast cancer cells that in turn overproduce this cytokine to create a local immunosuppressive environment that fosters tumor growth and exacerbates the invasive and metastatic behavior of the tumor cells themselves. Smads-mediated cross-talk with the estrogen receptor has been implied to play an important role in development and/or progression of breast cancer. We investigated how TGF-β regulates ERα-induced gene transcription and potential mechanisms of frequent TGF-β resistance in breast cancer. Effect of TGF-β on ERα-mediated gene transcription was investigated in breast cancer cell lines using transient transfection, real-time PCR, sequential DNA precipitation, and small interfering RNA assays. The expression of Smads on both human breast cancer cell lines and ERα-positive human breast cancer tissue was evaluated by immunofluorescence and immunohistochemical assays. A complex of Smad3/4 mediates TGF-β inhibition of ERα-mediated estrogenic activity of gene transcription in breast cancer cells, and Smad4 is essential and sufficient for such repression. Either overexpression of Smad3 or inhibition of Smad4 leads to the "switch" of TGF-β from a repressor to an activator. Down-regulation and abnormal cellular distribution of Smad4 were associated with some ERα-positive infiltrating human breast carcinoma. There appears a dynamic change of Smad4 expression from benign breast ductal tissue to infiltrating ductal carcinoma. These results suggest that aberrant expression of Smad4 or disruption of Smad4 activity lead to the loss of TGF-β suppression of ERα transactivity in breast cancer cells.
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      description:TGF-β resistance often develops in breast cancer cells that in turn overproduce this cytokine to create a local immunosuppressive environment that fosters tumor growth and exacerbates the invasive and metastatic behavior of the tumor cells themselves. Smads-mediated cross-talk with the estrogen receptor has been implied to play an important role in development and/or progression of breast cancer. We investigated how TGF-β regulates ERα-induced gene transcription and potential mechanisms of frequent TGF-β resistance in breast cancer. Effect of TGF-β on ERα-mediated gene transcription was investigated in breast cancer cell lines using transient transfection, real-time PCR, sequential DNA precipitation, and small interfering RNA assays. The expression of Smads on both human breast cancer cell lines and ERα-positive human breast cancer tissue was evaluated by immunofluorescence and immunohistochemical assays. A complex of Smad3/4 mediates TGF-β inhibition of ERα-mediated estrogenic activity of gene transcription in breast cancer cells, and Smad4 is essential and sufficient for such repression. Either overexpression of Smad3 or inhibition of Smad4 leads to the "switch" of TGF-β from a repressor to an activator. Down-regulation and abnormal cellular distribution of Smad4 were associated with some ERα-positive infiltrating human breast carcinoma. There appears a dynamic change of Smad4 expression from benign breast ductal tissue to infiltrating ductal carcinoma. These results suggest that aberrant expression of Smad4 or disruption of Smad4 activity lead to the loss of TGF-β suppression of ERα transactivity in breast cancer cells.
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