Purpose of review:
TGF-β acts as a potent driver of cancer progression through the induction of epithelial-mesenchymal transition (EMT), in which epithelial cells acquire mesenchymal phenotype, leading to enhanced motility and invasion. Recent reports highlight the fundamental roles of TGF-β-induced EMT in multiple aspects of cancer progression. In this review, we focus on the novel insights into the roles of TGF-β-induced EMT in cancer progression and the underlying mechanisms that enable TGF-β to activate this epithelial plasticity response at transcription, translation, and posttranslational levels.
Smad-mediated transcription regulation is known to activate TGF-β-induced EMT. More recently, novel mechanisms of epigenetic control, alternative splicing, miRNAs, translation control, and posttranslational modifications have been shown to play key roles in the control of EMT. In addition to initiating carcinoma cell invasion, TGF-β-induced EMT can guide cancer cells to de-differentiate and gain cancer stem-cell-like properties. EMT also allows the generation of stromal cells that support and instruct cancer progression.
The differentiation plasticity of epithelial cells that mediates TGF-β-induced EMT and reversion from mesenchymal to epithelial phenotype are increasingly seen as integral aspects of cancer progression that contribute to survival and dissemination of cancer cells. Further mechanistic insights under physiological conditions may lead to new therapeutic or prognostic strategies in cancer treatment.
"IF: 0.926 put forward . Whereafter, tumor stem cells have been isolated from acute myeloid leukemia, breast cancers and brain tumors (such as astrocytic tumors) . Therefore, this study studied on the heat shock protein (HSP) HSP90 and SIR3, both induced epithelial cell mesenchymal transdifferentiation and enhanced tumor stem cell characteristics, so as to promote the occurrence and development of liver cancer, and provide a theoretical reference value for the subsequent treatment of liver cancer. "
"The loss of ERα expression or function elicits EMT programs in MECs  , as does activation of the TGF-β signaling system   . As such, we monitored the extent to which Deptor expression is downregulated in NMuMG cells stimulated to undergo EMT programs by TGF-β or by overexpression of either PyMT, Twist, or β3 integrin   . "
"Thus, EMT is a pre-requisite for the advanced stage cancer cells to gain the invasive characteristics. Whereas TGFβ1 activity is well known to be associated with EMT  , the mediators of TGFβ1- induced EMT are still to be identified. P21 activated kinases (Paks) are the major downstream effectors of small GTPases Rac and cdc42, which are involved in the actin-based cytoskeletal remodeling  . "
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