Institute of Clinical Medicine, Taizhou People's Hospital Affiliated to Nantong University, Taizhou, 225300, Jiangsu, China.
The Department of Obstetrics and Gynecology, Taizhou People's Hospital Affiliated to Nantong University, Taizhou, 225300, Jiangsu, China.
Hum Cell. 2021 Mar;34(2):579-587. doi: 10.1007/s13577-020-00469-w. Epub 2021 Jan 5.
Ovarian cancer (OC) is a highly malignant tumor. X inactive specific transcript (XIST) was identified as a cancer-related gene, while its therapeutic effect in OC was poorly defined. The present study was designed to investigate the effectual corollary of the lncRNA XIST in OC. RT-qPCR was used to detect the XIST and miR-106a expression levels of OC tissues and cell lines. OC cell apoptosis and proliferation were detected by flow cytometry, colony formation, and CCK-8 assays. Moreover, bioinformatics analysis was used to predict the targeted miRNA of XIST. The dual-luciferase reporter and RNA pull-down assays were then used to verify the interaction between miR-106a and XIST. OC xenograft nude mice were raised to measure tumor growth. Notably, OC tissues and cells exhibited low XIST levels and high miR-106a levels. The XIST upregulation decreased the OVCAR3 and CAOV3 cell proliferation and inversely promoted cell apoptosis. miR-106a targeted the XIST. Also, the miR-106a overexpression reversed the inhibitory effects of XIST on OC cell proliferation and apoptosis. Our in vivo results suggested that XIST was involved in tumor growth deceleration, while the miR-106a reversed the effect. To conclusion, the present study demonstrated that XIST suppressed OC development via sponging miR-106a both in vitro and in vivo.
卵巢癌（OC）是一种高度恶性肿瘤。X 失活特异性转录物（XIST）被鉴定为一种与癌症相关的基因，但其在 OC 中的治疗效果尚不清楚。本研究旨在探讨长非编码 RNA XIST 在 OC 中的有效相关性。RT-qPCR 用于检测 OC 组织和细胞系中的 XIST 和 miR-106a 表达水平。通过流式细胞术、集落形成和 CCK-8 测定检测 OC 细胞凋亡和增殖。此外，还进行了生物信息学分析以预测 XIST 的靶向 miRNA。然后使用双荧光素酶报告和 RNA 下拉测定来验证 miR-106a 和 XIST 之间的相互作用。培养 OC 异种移植裸鼠以测量肿瘤生长。值得注意的是，OC 组织和细胞中 XIST 水平较低，miR-106a 水平较高。XIST 的上调降低了 OVCAR3 和 CAOV3 细胞的增殖，并反向促进了细胞凋亡。miR-106a 靶向 XIST。此外，miR-106a 的过表达逆转了 XIST 对 OC 细胞增殖和凋亡的抑制作用。我们的体内结果表明，XIST 通过在体外和体内吸附 miR-106a 参与肿瘤生长减速。总之，本研究表明 XIST 通过海绵 miR-106a 抑制 OC 的发展，无论是在体外还是体内。
