MiR-17-5p Up-Regulates YES1 to Modulate the Cell Cycle Progression and Apoptosis in Ovarian Cancer Cell Lines

• Published in: Journal of cellular biochemistry Vol. 116; no. 6; pp. 1050 - 1059
• Main Authors: Li, Lan, He, Li, Zhao, Jian-Li, Xiao, Jing, Liu, Min, Li, Xin, Tang, Hua
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01.06.2015; Wiley Subscription Services, Inc
• Subjects: Apoptosis - genetics; Apoptosis - physiology; Blotting, Western; CELL CYCLE; Cell Cycle - genetics; Cell Cycle - physiology; Cell Line, Tumor; Female; Flow Cytometry; Humans; MICRORNA; MicroRNAs - genetics; MicroRNAs - metabolism; MiR-17-5P; OVARIAN CANCER; Ovarian Neoplasms - genetics; Ovarian Neoplasms - metabolism; Proto-Oncogene Proteins c-yes - genetics; Proto-Oncogene Proteins c-yes - metabolism; Real-Time Polymerase Chain Reaction; TARGET GENE; YES1; OVARIAN CANCER; CELL CYCLE; YES1; TARGET GENE; MiR-17-5P; MICRORNA
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.25060

ABSTRACT MicroRNAs (miRNAs) are small, non‐coding RNAs that participate in the regulation of gene expression. Although many studies have demonstrated the involvement of miR‐17–5p in different cancers, little is known to its function in ovarian cancer. In this study, we demonstrated that overexpression of miR‐17–5p was able to enhance cell proliferation by promoting G1/S transition of the cell cycle and suppressing apoptosis in ES‐2 and OVCAR3 cell lines, whereas inhibition of miR‐17–5p yielded the reverse phenotype. YES1 was identified as a novel target gene of miR‐17–5p. Moreover, miR‐17–5p was found to directly bind to the 3′UTR of YES1 mRNA and up‐regulated its expression. Furthermore, knockdown of YES1 led to the suppression of proliferation and induced cell cycle arrest in ES‐2 and OVCAR3 cells. Ectopic expression of YES1 was able to reverse the effects of miR‐17–5p inhibition. Collectively, our results indicated that miR‐17–5p might play a role in human ovarian cancer by up‐regulating YES1 expression. J. Cell. Biochem. 116: 1050–1059, 2015. © 2015 Wiley Periodicals, Inc.