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Upregulated microRNA-224 promotes ovarian cancer cell proliferation by targeting KLLN

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Abstract

Human epithelial ovarian cancer is a complex disease, with low 5-yr survival rate largely due to the terminal stage at diagnosis in most patients. MicroRNAs play critical roles during epithelial ovarian cancer progression in vivo and have also been shown to regulate characteristic of ovarian cancer cell line in vitro. Alterative microRNA-224 (microRNA-224) expression affects human epithelial ovarian cancer cell survival, apoptosis, and metastasis. However, people know little about the effects of microRNA-224 on epithelial ovarian cancer cell proliferation. In the current study, we found that the microRNA-224 expression level of human syngeneic epithelial ovarian cancer cells HO8910 (low metastatic ability) was lower than that of HO8910PM (high metastatic ability). Furthermore, microRNA-224 was confirmed to target KLLN in HO8910 and HO8910PM. The known KLLN downstream target cyclin A was regulated by microRNA-224 in HO8910 and HO8910PM. In addition, overexpression of microRNA-224 enhanced the proliferation abilities of HO8910 and knockdown of microRNA-224 suppressed the proliferation abilities of HO8910PM by KLLN-cyclin A pathway. Our results provide new data about microRNAs and their targets involved in proliferation of epithelial ovarian cancer cells by modulating the downstream signaling.

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Acknowledgments

This research was funded by Natural Science Foundation of Anhui Province (CN) (1608085QH199), Natural Science Foundation of Bengbu Medical College (CN) (BYKY1406ZD and BYKY1444) and National Undergraduate Training Program for Innovation and Entrepreneurship of China (201410367033).

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Correspondence to Meng Liang.

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Meng Liang designed the experiments and drafted this manuscript. Ke Hu and Meng Liang carried out the experiments and approved this manuscript.

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The authors declare that they have no competing interests.

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Editor: Tetsuji Okamoto

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Hu, K., Liang, M. Upregulated microRNA-224 promotes ovarian cancer cell proliferation by targeting KLLN. In Vitro Cell.Dev.Biol.-Animal 53, 149–156 (2017). https://doi.org/10.1007/s11626-016-0093-2

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