Department of Laboratory, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Department of Gynecology, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Reprod Biol. 2022 Jun;22(2):100610. doi: 10.1016/j.repbio.2022.100610. Epub 2022 Mar 18.
Accumulating evidence has verified that the aberrant expression level of miR-493-3p is often associated with the occurrence of numerous cancers. Nevertheless, the expression level and effect of this microRNA in ovarian cancer (OC) remain largely unclear. Therefore, the molecular function of miR-493-3p in OC progression was systematically investigated in this study. The expression of miR-493-3p and DPY30 was assessed by qRT-PCR. The protein expression level of DPY30 in cell lines was further assessed by western blot. Cell viability was respectively examined in vitro functional experiments including CCK-8 assay, EdU assay, wound healing assay, colony formation and apoptosis assays as well as the scratch test and transwell assay. Bioinformatics analysis and luciferase reporter assays were performed to predict and clarity of the correlation between miR-493-3p and DPY30. The expression of miR-493-3p was significantly reduced in OC tissues and cells. Functional experimental results showed that miR-493-3p suppressed cellular proliferation, migration, invasion, but promoted apoptosis in OC cells. Mechanistically, we also confirmed that DPY30 could be directly targeted by miR-493-3p based on bioinformatics and dual-luciferase reporter analysis. Rescue experiments results indicated that the inhibitory effect of miR-493-3p on cellular proliferation, migration and invasion and the promotive effect of miR-493-3p on apoptosis was abolished by DPY30 overexpression. Our findings demonstrated the antitumor effect of miR-493-3p through targeting DPY30 in ovarian cancer, indicating that miR-493-3p might represent a promising target for ovarian cancer diagnosis and treatment.
越来越多的证据证实，miR-493-3p 的异常表达水平通常与许多癌症的发生有关。然而，这种 miRNA 在卵巢癌（OC）中的表达水平和作用在很大程度上仍不清楚。因此，本研究系统地研究了 miR-493-3p 在 OC 进展中的分子功能。通过 qRT-PCR 评估 miR-493-3p 和 DPY30 的表达。通过 Western blot 进一步评估细胞系中 DPY30 的蛋白表达水平。在体外功能实验中分别检测细胞活力，包括 CCK-8 测定、EdU 测定、划痕试验、transwell 测定和伤口愈合试验以及集落形成和凋亡测定。进行生物信息学分析和荧光素酶报告基因测定，以预测和阐明 miR-493-3p 和 DPY30 之间的相关性。miR-493-3p 在 OC 组织和细胞中的表达明显降低。功能实验结果表明，miR-493-3p 抑制 OC 细胞的增殖、迁移和侵袭，但促进凋亡。基于生物信息学和双荧光素酶报告基因分析，我们还证实 DPY30 可被 miR-493-3p 直接靶向。挽救实验结果表明，miR-493-3p 对细胞增殖、迁移和侵袭的抑制作用以及 miR-493-3p 对凋亡的促进作用被 DPY30 过表达所消除。我们的研究结果表明，miR-493-3p 通过靶向 DPY30 在卵巢癌中发挥抗肿瘤作用，表明 miR-493-3p 可能成为卵巢癌诊断和治疗的有前途的靶点。
