Affiliations: [a] Gynecological Department, Wuhan Hanyang Hospital, Wuhan, Hubei, China | [b] Department of Oncology, Chengdu Fifth People’s Hospital, Chengdu, Sichuan, China | [c] Department of Gynecology, The Qingdao Hiser Hospital, Qingdao, Shandong, China | [d] Department of Obstetrics and Gynecology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China | [e] Department of Reproductive Medicine, the Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China
Correspondence:
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Corresponding author: Zhiming Zhao, Department of Reproductive Medicine, the Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang, Hebei, China. E-mail: [email protected].
Note: [1] Ming Ni and Qin Yan contributed equally to the article.
Abstract: BACKGROUND: The dysregulation of microRNA-802 (miR-802) has crucial roles in cancer progression. Nevertheless, the bio-function of miR-802 in cervical cancer remains unclear. OBJECTIVE: Hence, we illuminated the potential roles of miR-802 in cervical cancer cell growth, migration, and invasion. METHODS: The levels of miR-802 and myosin regulatory light chain interacting protein (MYLIP) were measured using qRT-PCR assay. The potential effects of miRNA-802 on cervical cancer cell proliferation and metastatic phenotypes were determined using CCK-8, colony formation, wound healing and Transwell invasion assays. MYLIP was validated as a downstream target gene of miRNA-802 using bioinformatics analysis tool and luciferase report gene assay. The impact of miR-802 on the growth of cervical cancer cell in vivo was analyzed using xenograft model. The expression of MYLIP was measured by western blotting and immunohistochemistry (IHC). RESULTS: MiRNA-802 was distinctly down-regulated in cervical cancer cells as well as clinical cervical cancer samples. Upregulation of miRNA-802 significantly inhibited the growth and aggressiveness of cervical cancer cell. Additional, MYLIP was a functional target of miR-802. MYLIP was ovrerexpressed in cervical cancer and MYLIP level was negatively associated with the level of miR-802. Overexpression of MYLIP eliminated the inhibitory effects of miR-802 on growth and metastatic-related traits of cervical cancer cell. In vivo, miR-802 also markedly reduced the tumor growth of cervical cancer cell and decreased the expression of MYLIP. CONCLUSIONS: MiR-802 inhibits the growth and metastatic-related phenotypes of cervical cancer cell through targeting MYLIP.
