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TGF-β and cancer: Is Smad3 a repressor of hTERT gene?

机译：TGF-β和癌症：Smad3是hTERT基因的阻遏物吗？

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Transforming growth factor β (TGF-β) carries out tumor suppressor activity in epithelial and lymphoid cells, whereas telomerase is required for most cancers. Although the molecular mechanisms by which TGF-β acts as a tumor suppressor are yet to be fully established, a link between TGFb and its tumor suppressor activity by telomerase has been suggested. Recently, we have noted a novel mode of action for TGF-β through which human telomerase reverse transcriptase (hTERT) gene is repressed in immortal and neoplastic cells, confirming that one of the mechanisms underlying TGF-β suppression of tumor growth may be through inhibiting hTERT gene transcription. Moreover, the inhibition of hTERT gene by TGF-β suggests a cis action of the TGF-β signaling molecule Smad3 on hTERT promoter directly. This article examines our current understanding and investigation of TGF-β regulation of telomerase activity, and presents a model in which Smad3 participates in regulating hTERT gene transcription by acting as a repressor directly. Engineering the interface between Smad3 and hTERT gene may lead to a new strategy to inhibit telomerase activity in cancer.
机译：转化生长因子β（TGF-β）在上皮和淋巴样细胞中具有肿瘤抑制活性，而端粒酶是大多数癌症所必需的。尽管尚未完全确立TGF-β充当肿瘤抑制物的分子机制，但是已经提出了TGFb与其通过端粒酶抑制肿瘤活性之间的联系。最近，我们注意到了TGF-β的一种新的作用方式，通过该作用方式，可以在永生和赘生性细胞中抑制人类端粒酶逆转录酶（hTERT）基因，从而证实TGF-β抑制肿瘤生长的潜在机制之一可能是通过抑制hTERT基因转录。此外，TGF-β对hTERT基因的抑制表明TGF-β信号分子Smad3直接对hTERT启动子具有顺式作用。本文考察了我们目前对端粒酶活性的TGF-β调控的理解和研究，并提出了一个模型，其中Smad3通过直接充当阻遏物参与了hTERT基因转录的调控。工程Smad3和hTERT基因之间的接口可能导致抑制癌症端粒酶活性的新策略。

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