Department of Obstetrics and Gynecology, the Second Affiliated Hospital of Nantong University (First People's Hospital of Nantong City), Nantong, Jiangsu, 226001, China.
Acta Biochim Pol. 2022 Oct 22;69(4):745-751. doi: 10.18388/abp.2020_5987.
MicroRNA-650 (miR-650) has been shown to regulate the development of human cancers. The present study investigated the role of miR-650 in ovarian cancer by targeting Krüppel-like factor 12 (KLF12). The results showed a down-regulation of miR-650 in tissues and cell lines. Overexpression of miR-650 caused a substaining decrease in the viability of CAOV3 cells by promoting apoptotic cell death. In silico analysis and dual luciferase assay revealed KLF12 as a potential target of miR-650. Unlike miR-650, KLF12 showed a substantial up-regulation in ovarian cancer tissues and cell lines. However, miR-650 overexpression suppressed KLF12 expression posttranscriptionally. Intrestingly, KLF12 knockdown inhibited the viability of CAOV3 cells by promoting apoptotic cell death. However, the expression of KLF12 eliminated the tumor suppressing effects of miR-650 in CAOV3 cells. Additionally, KLF12 knockdown or miR-650 overexpression suppressed CAOV3 cell migration and invasion. However, KLF12 overexpression eliminated the inhibitory effects of miR-650 on the migration and invasion of CAOV3 cells. Taken together, these results suggest that miR-650/KLF12 axis regulates the viability, migration, and invasion of CAOV3 cells an0d may prove to be an important therapeutic taregt.
微小 RNA-650（miR-650）已被证明可以调节人类癌症的发展。本研究通过靶向 Krüppel 样因子 12（KLF12）来研究 miR-650 在卵巢癌中的作用。结果表明 miR-650 在组织和细胞系中下调。miR-650 的过表达通过促进凋亡细胞死亡导致 CAOV3 细胞活力持续下降。计算机分析和双荧光素酶报告基因实验显示 KLF12 是 miR-650 的潜在靶标。与 miR-650 不同，KLF12 在卵巢癌组织和细胞系中大量上调。然而，miR-650 的过表达在转录后抑制 KLF12 的表达。有趣的是，KLF12 的敲低通过促进凋亡细胞死亡抑制 CAOV3 细胞的活力。然而，KLF12 的表达消除了 miR-650 在 CAOV3 细胞中的肿瘤抑制作用。此外，KLF12 的敲低或 miR-650 的过表达抑制 CAOV3 细胞的迁移和侵袭。然而，KLF12 的过表达消除了 miR-650 对 CAOV3 细胞迁移和侵袭的抑制作用。总之，这些结果表明 miR-650/KLF12 轴调节 CAOV3 细胞的活力、迁移和侵袭，并且可能被证明是一个重要的治疗靶标。
