CUL4A functions as an oncogene in ovarian cancer and is directly regulated by miR-494
- Department of Obstetrics and Gynecology, The Fourth Affiliated Hospital of Nanchang University, Nanchang, 330003, Jiangxi Province (China)
- Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province (China)
- Department of Orthopedics, Huashan Hospital, Fudan University, Shanghai, 200040 (China)
- Department of Gastroenterology, The Third Affiliated Hospital of Nanchang University, Nanchang, 330003, Jiangxi Province (China)
Cullin 4A (CUL4A), as a well-defined oncogene, has been reported to be upregulated in ovarian cancer clinically. However, the biological functions of CUL4A and the molecular mechanism underlying its upregulation in ovarian cancer remains unknown throughly. Here, we show that expression of CUL4A is significantly higher in ovarian cancer tissues compared to corresponding non-cancerous tissues. Moreover, silencing of CUL4A by siRNA markedly inhibits cell proliferation, invasion and epithelial-mesenchymal transition (EMT). We identified CUL4A as a novel target gene of miR-494. Further investigations showed that miR-494 was remarkably downregulated and correlated with poor prognosis in ovarian cancer. Overexpression of miR-494 inhibited proliferation, migration, invasion and EMT of ovarian cancer cells by directly suppressing CUL4A expression. Therefore, our findings indicate that miR-494/CUL4A axis is important in the control of ovarian cancer tumorigenesis. - Highlights: • CUL4A is upregulated in ovarian cancer and knockdown of CUL4A inhibits cell proliferation, invasion and EMT. • MiR-494 directly targets CUL4A 3′UTR. • MiR-494 is frequently downregulated and correlated with poor prognosis in ovarian cancer. • CUL4A is involved in miR-494-induced tumor suppressive effects.
- OSTI ID:
- 22696714
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 480, Issue 4; Other Information: Copyright (c) 2016 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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