MEST induces Twist-1-mediated EMT through STAT3 activation in breast cancers.

The loss of imprinting of MEST has been linked to certain types of cancer by promoter switching. However, MEST-mediated regulation of tumorigenicity and metastasis are yet to be understood. Herein, we reported that MEST is a key regulator of signal pathway-mediated tumor metastasis. Enhanced MEST expression is significantly associated with pathogenesis of breast cancer patients. Also, MEST induces metastatic potential of breast cancer through induction of the EMT-TFs-mediated EMT program. Moreover, MEST leads to Twist-1 induction by activation and subsequently enables the induction of activation of the EMT program via the induction of duanyu18133 nuclear translocation. Furthermore, the c-terminal region of MEST was essential for duanyu18133 activation via the induction of complex formation. Finally, MEST is required for metastasis in an experimental metastasis model. These observations suggest that MEST is a promising target for intervention to prevent tumor metastasis.

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