MEST induces Twist-1-mediated EMT through STAT3 activation in breast cancers
- Authors
- Kim, Min Soo; Lee, Hyun Sook; Kim, Yun Jae; Lee, Do Yup; Kang, Sung Gyun; Jin, Wook
- Issue Date
- Dec-2019
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- CELL DEATH AND DIFFERENTIATION, v.26, no.12, pp.2594 - 2606
- Journal Title
- CELL DEATH AND DIFFERENTIATION
- Volume
- 26
- Number
- 12
- Start Page
- 2594
- End Page
- 2606
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/17890
- DOI
- 10.1038/s41418-019-0322-9
- ISSN
- 1350-9047
- 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.
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