Knockdown of SNHG1 inhibits cervical cancer growth through sponging miR-194 to regulate HCCR

Abstract

Aim

To investigate the mechanism of small nucleolar RNA host gene 1 (SNHG1) in cervical cancer (CC). Methods: The expression of SNHG1, miR-194 and human cervical cancer oncogene (HCCR) in CC tissues and cells was detected using qRT-PCR and western blot. The interaction among the three molecules was measured using dual-luciferase reporter assay and RNA immunoprecipitation assay. The function of SNHG1 in CC cells was detected by CKK-8 assay and flow cytometry analysis. Results: SNHG1 was highly expressed in CC tissues and CC cell lines. Knockdown of SNHG1 inhibited CC cell proliferation and enhanced the ability of cell apoptosis. Mechanism investigation revealed that SNHG1 modulated HCCR expression via acting as a competing endogenous RNA of miR-194. Moreover, miR-194 inhibitor changed the effects of si-SNHG1 on CC cells growth. In vivo experiment, silencing of SNHG1 suppressed CC tumor growth by modulating miR-194/HCCR axis. Conclusion: Knockdown of SNHG1 inhibited CC progression by targeting HCCR via sponging with miR-194.

摘要

目的：探讨小核仁RNA宿主基因1 (SNHG1) 在宫颈癌 (CC) 中的作用机制。

方法：采用qRT-PCR和Western blot方法检测SNHG1、miR-194和人宫颈癌癌基因 (HCCR) 在CC组织和细胞中的表达。使用双荧光素酶报告实验和RNA免疫沉淀实验来检测三种分子间的相互作用。采用CKK-8比色法和流式细胞仪检测SNHG1在CC细胞中的功能。结果：SNHG1在CC组织和CC细胞系中高表达。SNHG1基因敲除可抑制CC细胞增殖, 增强细胞凋亡能力。机制研究表明, SNHG1通过作为miR-194的内源竞争RNA来调控HCCR的表达。此外, miR-194抑制剂改变了si-SNHG1对CC细胞生长的影响。体内实验表明, 沉默SNHG1通过调节miR-194/HCCR轴抑制CC肿瘤生长。结论：敲除SNHG1可以通过与miR-194配对来靶向HCCR, 从而抑制CC进程。

Keywords:

• Cervical cancer
• SNHG1
• miR-194
• HCCR
• growth

Disclosure statement

No potential conflict of interest was reported by the author(s).