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首页> 外文期刊>Signal transduction: Receptors, mediators and genes: Official journal of the Signal Transduction Society >Recent advances in TGFβ-regulated transcription during carcinogenesis
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Recent advances in TGFβ-regulated transcription during carcinogenesis

机译：癌变过程中TGFβ调控转录的最新进展

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摘要

The multifunctional activities of transforming growth factor-beta (TGFβ) endow it with both tumor suppressor and tumor promoting activities, depending on the stage of carcinogenesis and the cellular activation state. In early tumor stages, TGFβ inhibits epithelial cell growth through induction of apoptosis and transcriptional regulation of cell cycle controlling genes. During tumor progression, however, many cancer cells escape from TGFβ-induced growth inhibition and, instead, respond to TGFβ with increased malignancy. TGFβ stimulates tumor promotion particularly in those tumor cells in which Smad-signaling remains functional and through transcriptional regulation of gene expression. Thus, loss of sensitivity to growth inhibition by TGFβ is not synonymous with complete loss of TGFβ signaling. Rather, it suggests that tumor cells gain advantage by selective inactivation of TGFβ tumor suppressor activities while retaining its tumor promoting functions. In this review we focus on novel aspects in TGFβ signaling and transcription and in particular on the role of Smad-interacting transcription factors. We also summarize recent advances in both cytoplasmic and nuclear crosstalk mechanisms between Smad and non-Smad signaling pathways and how this interaction results in the fine-tuning of Smad-mediated transcription during cancer progression. This knowledge will help to better understand the molecular mechanisms responsible for the switch of TGFβ from a tumor suppressor to a tumor promotor.
机译：转化生长因子-β（TGFβ）的多功能活性使其具有抑癌和促肿瘤活性，具体取决于癌变阶段和细胞激活状态。在肿瘤的早期阶段，TGFβ通过诱导细胞凋亡和细胞周期控制基因的转录调控来抑制上皮细胞的生长。然而，在肿瘤进展期间，许多癌细胞逃避了TGFβ诱导的生长抑制，而是以增加的恶性反应对TGFβ作出反应。 TGFβ尤其在那些Smad信号仍然起作用并通过基因表达的转录调控的肿瘤细胞中刺激肿瘤的生长。因此，对TGFβ抑制生长的敏感性的丧失与TGFβ信号传导的完全丧失并不等同。相反，这表明肿瘤细胞通过选择性失活TGFβ肿瘤抑制活性而获得优势，同时保留其肿瘤促进功能。在这篇综述中，我们专注于TGFβ信号传导和转录的新方面，尤其是与Smad相互作用的转录因子的作用。我们还总结了Smad和非Smad信号通路之间的细胞质和核串扰机制的最新进展，以及这种相互作用如何导致Smad介导的转录在癌症进展过程中的微调。这些知识将有助于更好地理解导致TGFβ从肿瘤抑制物转变为肿瘤促进剂的分子机制。

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