Zhang R-R, Wang L-M, Shen J-J
Department of Gynecology, The Ninth People's Hospital of Suzhou, Suzhou, China.
Eur Rev Med Pharmacol Sci. 2020 May;24(9):4671-4678. doi: 10.26355/eurrev_202005_21154.
The purpose of this study was to explore the role of microRNA-32 (miR-32) in ovarian cancer and the possible underlying mechanism.
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.
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.
Acting as a suppressor gene, miR-32 inhibited the malignant behaviors of ovarian cancer cells by regulating its target gene BTLA.
本研究旨在探讨微小RNA - 32（miR - 32）在卵巢癌中的作用及可能的潜在机制。
收集我院确诊为卵巢癌的100例患者的癌组织。采用定量实时聚合酶链反应（qRT - PCR）检测卵巢组织中miR - 32及其靶基因的表达水平。采用MTT（3 -（4,5 - 二甲基噻唑 - 2 - 基）- 2,5 - 二苯基四氮唑溴盐）法检测卵巢癌细胞的增殖情况。同时，分别采用Transwell实验和伤口愈合实验评估卵巢癌细胞的迁移和侵袭能力。利用生物信息学方法（包括TargetScan、miRDB和microRNA）预测miR - 32的靶基因。此外，进行双荧光素酶报告基因实验以验证结合关系。
miR - 32在卵巢癌组织和细胞中均显著下调。miR - 32的过表达显著抑制了卵巢癌细胞的增殖、迁移和侵袭。筛选出B和T淋巴细胞相关分子（BTLA）作为miR - 32的靶基因。此外，BTLA可抵消miR - 32对卵巢癌细胞的作用。
作为一种抑癌基因，miR - 32通过调控其靶基因BTLA抑制卵巢癌细胞的恶性行为。
