MicroRNA-497 suppresses angiogenesis by targeting vascular endothelial growth factor A through the PI3K/AKT and MAPK/ERK pathways in ovarian cancer

• Published in: Oncology reports Vol. 32; no. 5; pp. 2127 - 2133
• Main Authors: WANG, WEI, REN, FANG, WU, QINGHUA, JIANG, DAZHI, LI, HONGJUN, SHI, HUIRONG
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.11.2014; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Adult; Aged; Aged, 80 and over; AKT; Angiogenesis; Binding sites; Breast cancer; Cancer; Cancer therapies; Cell growth; Cystadenocarcinoma, Serous - blood supply; Cystadenocarcinoma, Serous - genetics; Cystadenocarcinoma, Serous - pathology; ERK; Female; Gene Expression Regulation, Neoplastic; Humans; Immunoglobulins; MAP Kinase Signaling System; Metastasis; MicroRNA; MicroRNAs - genetics; MicroRNAs - metabolism; Middle Aged; miR-497; Neovascularization; Neovascularization, Pathologic - genetics; Neovascularization, Pathologic - metabolism; Oncology, Experimental; Ovarian cancer; ovarian carcinoma; Ovarian Neoplasms - blood supply; Ovarian Neoplasms - genetics; Ovarian Neoplasms - pathology; Patients; Physiological aspects; Proteins; Vascular endothelial growth factor; Vascular Endothelial Growth Factor A - genetics; Vascular Endothelial Growth Factor A - metabolism; VEGFA; United States > US
• ISSN: 1021-335X; 1791-2431
• DOI: 10.3892/or.2014.3439

MicroRNAs (miRNAs) have been shown to play an important role in diverse biological processes and cancer progression. The objective of the present study was to investigate the role of miR-497 in ovarian cancer angiogenesis. We found that miR-497 expression was downregulated in human ovarian cancer tissues, and the low miR-497 expression was significantly associated with increased angiogenesis. Functionally, exogenous expression of miR-497 suppressed the ability of ovarian cancer cells to promote capillary tube formation of endothelial cells. We further disclosed that miR-497 exerted its function of anti-angiogenesis by suppressing VEGFA expression in ovarian cancer cells and, in turn, impairing the VEGFR2-mediated PI3K/AKT and MAPK/ERK pathways. Our findings suggest that downregulation of miR-497 may contribute to angiogenesis in ovarian cancer. miR-497 may be a promising candidate target for prevention and treatment of ovarian cancer.