MEST induces Twist-1-mediated EMT through STAT3 activation in breast cancers
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Title
- MEST induces Twist-1-mediated EMT through STAT3 activation in breast cancers
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Author(s)
- Kim, Min Soo; Lee, Hyun Sook; Kim, Yun Jae; Lee, Do Yup; Kang, Sung Gyun; Jin, Wook
- KIOST Author(s)
- Lee, Hyun Sook(이현숙); Kim, Yun Jae(김윤재); Kang, Sung Gyun(강성균)
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Alternative Author(s)
- 이현숙; 김윤재; 강성균
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Publication Year
- 2019-12
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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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ISSN
- 1350-9047
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URI
- https://sciwatch.kiost.ac.kr/handle/2020.kiost/449
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DOI
- 10.1038/s41418-019-0322-9
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Bibliographic Citation
- CELL DEATH AND DIFFERENTIATION, v.26, no.12, pp.2594 - 2606, 2019
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Publisher
- NATURE PUBLISHING GROUP
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Subject
- TO-MESENCHYMAL TRANSITION; EXPRESSION; PEG1/MEST; CELLS; GENE; METASTASIS; GROWTH; PLAYS; INSIGHTS; TWIST
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Type
- Article
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Language
- English
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Document Type
- Article
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