TRPM7 is required for ovarian cancer cell growth, migration and invasion
- The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013 (China)
- Department of Obstetrics and Gynaecology, Xiangya Hospital, Central South University, Changsha 410078 (China)
- Department of Basic Medical Science, Yongzhou Vocational Technical College, Yong Zhou 425100 (China)
- Department of Histology and Embryology, School of Basic Medical Sciences, Central South University, Changsha 410013 (China)
Highlights: • Silence of TRPM7 in ovarian cancer cells inhibits cell proliferation, migration and invasion. • Silence of TRPM7 decreases phosphorylation levels of Akt, Src and p38 in ovarian cancer cells. • Silence of TRPM7 increases expression of filamentous actin and number of focal adhesions in ovarian cancer cells. - Abstract: Our previous study demonstrated that the melastatin-related transient receptor potential channel 7 (TRPM7) was highly expressed in ovarian carcinomas and its overexpression was significantly associated with poor prognosis in ovarian cancer patients. However, the function of TRPM7 in ovarian cancer is mostly unknown. In this study, we examined the roles of TRPM7 in ovarian cancer cell proliferation, migration and invasion. We found that short hairpin RNA interference-mediated silence of TRPM7 significantly inhibited cell proliferation, colony formation, migration and invasion in multiple ovarian cancer cell lines. Mechanistic investigation revealed that silence of TRPM7 decreased phosphorylation levels of Akt, Src and p38 and increased filamentous actin and focal adhesion number in ovarian cancer cells. Thus, our results suggest that TRPM7 is required for proliferation, migration and invasion of ovarian cancer cells through regulating multiple signaling transduction pathways and the formation of focal adhesions.
- OSTI ID:
- 22416845
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 454, Issue 4; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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