The aim of this study was to investigate the effect role and mechanism of miR-30b-3p on ovarian cancer cells biological function. The expression of miR-30b-3p was detected in ovarian cancer cell lines and normal ovarian epithelial cell line by qRT-PCR. Mir-30b-3p mimic was transfected into OVCAR3 cells. Cell-counting kit-8 (CCK-8) assay was conducted to explore the effect of mir-30b-3p on the OVCAR3 cells’ proliferation. Cell cycle and apoptosis were detected by Flow cytometry. Cell invasion ability was detected by Transwell test. The regulation of putative target of miR-30b-3p was verified by double luciferase reporter assays and Western blot. We found that miR-30b-3p was downregulated in OVCAR3 cells. Overexpression of miR-30b-3p suppressed proliferation, promoted apoptosis, slowed cell cycle and inhibited migration and invasion of OVCAR3 cells. Bioinformatics analysis identified 3′-untranslated region (3′UTR) of Collagen triple helix repeat-containing 1 (CTHRC1) as the presumed binding site for miR-30b-3p. Detection of double luciferase reporter and Western-Blot result confirmed that CTHRC1 was the target gene of miR-30b-3p. Furthermore, E-cadherin, β-cadherin and Vimentin protein expression level were changed after transfection of miR-30b-3p. miR-30b-3p function as an anti-cancer gene. Overexpression of miR-30b-3p can inhibit the biological function of ovarian cancer cells. MiR-30b-3p targets CTHRC1 gene plays an important role in epithelial–mesenchymal transformation (EMT), and supports miR-30b-3p as a potential biological indicator for ovarian cancer in the future.

中文翻译：

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Mir-30b-3p通过靶向CTHRC1基因影响卵巢癌细胞的迁移和侵袭功能

这项研究的目的是研究miR-30b-3p对卵巢癌细胞生物学功能的作用和机制。通过qRT-PCR检测miR-30b-3p在卵巢癌细胞系和正常卵巢上皮细胞系中的表达。将Mir-30b-3p模拟物转染到OVCAR3细胞中。进行细胞计数试剂盒8（CCK-8）分析，以研究mir-30b-3p对OVCAR3细胞增殖的影响。流式细胞仪检测细胞周期和凋亡。通过Transwell测试检测细胞侵袭能力。miR-30b-3p假定的靶标的调控通过双重荧光素酶报告基因分析和Western印迹法进行验证。我们发现miR-30b-3p在OVCAR3细胞中被下调。miR-30b-3p的过表达抑制增殖，促进凋亡，减慢细胞周期并抑制OVCAR3细胞的迁移和侵袭。生物信息学分析确定了含胶原三螺旋重复序列1（CTHRC1）的3'非翻译区（3'UTR）作为miR-30b-3p的假定结合位点。双荧光素酶报告基因的检测和Western-Blot结果证实，CTHRC1是miR-30b-3p的靶基因。转染miR-30b-3p后，E-cadherin，β-cadherin和Vimentin蛋白的表达水平发生了改变。miR-30b-3p可作为抗癌基因。miR-30b-3p的过度表达可以抑制卵巢癌细胞的生物学功能。MiR-30b-3p靶向CTHRC1基因在上皮-间质转化（EMT）中发挥重要作用，并支持miR-30b-3p作为将来卵巢癌的潜在生物学指标。