目的:CERS6反义RNA1(CERS6-AS1),一种长非编码RNA(lncRNA),在多种癌症的恶性进展中起作用。然而,目前尚不清楚它是否会影响宫颈癌(CC)细胞的恶性行为。
方法:通过qRT-PCR评估CC中的CERS6-AS1和miR-195-5p表达。CCK-8,caspase-3活性,划痕,和Transwell测定进行检测CC细胞活力,caspase-3活性,迁移,和体外侵袭。设计肿瘤异种移植实验以研究CC肿瘤在体内的生长。RIP和荧光素酶报告基因实验验证了CERS6-AS1和miR-195-5p之间的关系。
结果:在CC中观察到CERS6-AS1过表达和miR-195-5p水平差。抑制CERS6-AS1损害了生存能力,入侵,和CC细胞的迁移,促进细胞凋亡,抑制肿瘤生长.就潜在机制而言,CERS6-AS1,作为竞争性内源性RNA(ceRNA),参与调节CC细胞中miR-195-5p水平。功能上,miR-195-5p干扰减弱了CERS6-AS1对CC细胞恶性行为的抑制作用。
结论:CERS6-AS1在CC中充当癌基因,体内和体外,通过负调控miR-195-5p。
OBJECTIVE: CERS6 antisense RNA 1 (CERS6-AS1), a long non-coding RNA (lncRNA), plays a role in the malignant progression of a variety of cancers. However, it is unclear whether it affects the malignant behavior of cervical cancer (CC) cells.
METHODS: CERS6-AS1 and miR-195-5p expression was estimated in CC via qRT-PCR. CCK-8, caspase-3 activity, scratch, and Transwell assays were performed to detect CC cell viability, caspase-3 activity, migration, and invasion in vitro. A tumor xenograft experiment was designed to study the growth of CC tumors in vivo. RIP and luciferase reporter experiments verified the relationship between CERS6-AS1 and miR-195-5p.
RESULTS: CERS6-AS1 overexpression and poor miR-195-5p levels were observed in CC. Inhibition of CERS6-AS1 impaired the viability, invasion, and migration of CC cells, promoted apoptosis, and suppressed tumor growth. In terms of the underlying mechanism, CERS6-AS1, as a competitive endogenous RNA (ceRNA), participated in the regulation of miR-195-5p levels in CC cells. Functionally, miR-195-5p interference attenuated the inhibitory effect of CERS6-AS1 on the malignant behaviors of CC cells.
CONCLUSIONS: CERS6-AS1 acts as an oncogene in CC, in vivo and in vitro, by negatively regulating miR-195-5p.