| Literature DB >> 30903102 |
Min Soo Kim1, Hyun Sook Lee2,3, Yun Jae Kim2,3, Do Yup Lee4, Sung Gyun Kang5,6, Wook Jin7.
Abstract
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 IL-6/JAK/STAT3/Twist-1 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 STAT3 activation and subsequently enables the induction of activation of the EMT program via the induction of STAT3 nuclear translocation. Furthermore, the c-terminal region of MEST was essential for STAT3 activation via the induction of JAK2/STAT3 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.Entities:
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Year: 2019 PMID： 30903102 PMCID： PMC7224286 DOI： 10.1038/s41418-019-0322-9
Source DB: PubMed Journal: Cell Death Differ ISSN： 1350-9047 Impact factor: 15.828