Overexpression of miR-32 inhibits the proliferation and metastasis of ovarian cancer cells by targeting BTLA

R.-R. Zhang, L.-M. Wang, J.-J. Shen

Department of Gynecology, The Ninth People’s Hospital of Suzhou, Suzhou, China. 372417758@qq.com

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• Oncology

OBJECTIVE: The purpose of this study was to explore the role of microRNA-32 (miR-32) in ovarian cancer and the possible underlying mechanism.

PATIENTS AND METHODS: Ovarian cancer tissues were collected from 100 patients diagnosed with ovarian cancer in our hospital. Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was used to detect the expression levels of miR-32 and its target gene in ovarian tissues. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay was conducted to detect the proliferation of ovarian cancer cells. Meanwhile, the transwell and wound healing assays were used to evaluate the migration and invasion abilities of ovarian cancer cells, respectively. Bioinformatics (including TargetScan, miRDB, and microRNA) were used to predict the target genes of miR-32. Furthermore, The Dual-Luciferase reporter gene assay was performed to verify the binding relationship.

RESULTS: MiR-32 was significantly downregulated in both ovarian cancer tissues and cells. The overexpression of miR-32 significantly inhibited the proliferation, migration, and invasion of ovarian cancer cells. B and T lymphocyte associated (BTLA) was screened out as a target gene of miR-32. Furthermore, BTLA could counteract the effects of miR-32 on ovarian cancer cells.

CONCLUSIONS: Acting as a suppressor gene, miR-32 inhibited the malignant behaviors of ovarian cancer cells by regulating its target gene BTLA.

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