Long non-coding RNA (lncRNA) SNHG4 has been shown to be associated with the development of a variety of cancers. The purpose of this study was to investigate the effect of SNHG4 on cervical cancer (CC) and the corresponding mechanism. The qRT-PCR was used to determine the expressions of SNHG4 and miR-148a-3p in CC cell lines and tissues. Cell apoptosis and proliferation were measured by flow cytometry and MTT assay, respectively. The interaction between SNHG4, miR-148a-3p and c-Met was verified by bioinformatics, dual-luciferase reporter gene and RNA immunoprecipitation (RIP), and the effect of SNHG4 on the growth of CC tumor in vivo was explored. The expression of SNHG4 was increased in both CC cell lines and tissues, while the expression of miR-148a-3p was down-regulated. Meanwhile, silencing SNHG4 remarkably inhibited CC cell proliferation and promoted apoptosis. In addition, miR-148a-3p was a direct target gene of SNHG4, and down-regulation of miR-148a-3p could observably reverse the effect of silencing SNHG4 on the proliferation and apoptosis of CC cells. More importantly, SNHG4 could up-regulate the expression of c-Met by targeting and interacting with miR-148a-3p. Finally, in vivo experiments confirmed that silence SNHG4 down-regulated the expression of c-Met by promoting miR-148a-3p, and ultimately suppressed the growth of CC tumor in vivo. In conclusion, SNHG4 could be used as a competitive endogenous RNA to bind to miR-148a-3p, thereby up-regulating the expression of c-Met and ultimately promoting the progression of CC, which provided a potential therapeutic target for the targeted treatment of CC.
Keywords: Cervical cancer; c-Met; lncRNA SNHG4; miR-148a-3p.