Long non-coding RNA <i>SNHG4</i> promotes cervical cancer progression through regulating c-Met via targeting miR-148a-3p

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