Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p

被引:66
作者
Dong, Jing [1 ]
Wang, Qing [1 ]
Li, Li [2 ]
Zhang, Xiao-jin [1 ]
机构
[1] Fudan Univ, Obstet & Gynecol Hosp, Ctr Diag & Treatment Cerv Dis, Shanghai, Peoples R China
[2] Jiangyin Third Peoples Hosp, Dept Obstet & Gynecol, Jiangyin, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Snhg12; Cervical cancer; MiR-424-5p; Proliferation; Apoptosis; NEOADJUVANT CHEMOTHERAPY; PROLIFERATION; EXPRESSION; APOPTOSIS; MIGRATION; LNCRNA;
D O I
10.1159/000488045
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Cervical cancer, which is one of the most aggressive cancers affecting females, has high rates of recurrence and mortality. Small nucleolar RNA host gene 12 (SNHG12) is known to promote the progression of several cancers; however, its exact effects and molecular mechanisms in cervical cancer remain unknown. Methods: Real-time quantitative PCR was used to determine the expression level of SNHG12 in cervical cancer tissues and cell lines. Loss-of-function assays were performed to examine the effect of SNHG12 on the proliferation, apoptosis, migration and invasion of cervical cancer cells in vitro and tumor growth in vivo. Luciferase experiments were employed to explore the interactions between SNHG12 and miR-424-5p. Results: SNHG12 was found to be abnormally elevated in human cervical cancer tissues compared with paired adjacent normal tissues. Moreover, high SNHG12 expression in tumor tissues was significantly correlated with vascular involvement, lymph node metastasis, advanced FIGO stage and poor prognosis. Furthermore, the knockdown of SNHG12 was found to inhibit proliferation, migration and invasion of cervical cancer cells in vitro, and silencing SNHG12 was shown to suppress tumor growth in a nude mouse model. Mechanistic studies showed that SNHG12 functioned as an endogenous sponge for miR-4245p, thereby downregulating the expression of miR-424-5p in cervical cancer. Furthermore, the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion. Conclusion: In summary, our findings suggest that the tumor-promoting role of SNHG12 is to function as a molecular sponge, which negatively regulates miR-424-5p. These findings may provide a potent therapeutic target for cervical cancer. (C) 2018 The Author(s) Published by S Karger AG, Basel.
引用
收藏
页码:2086 / 2094
页数:9
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