Abstract
Increasing evidence indicates the important roles of long noncoding RNA (lncRNA) in the endometrial carcinoma (ECa). Here, we identified the roles of SNHG16 in the ECa proliferation and glycolysis, and revealed the underlying mechanism. Results presented that SNHG16 expression was increased in the ECa tissue and cells, and the ectopic SNHG16 overexpression was closely correlated with the poor survival rate and recurrence free survival of ECa. As regarding the upstream, transcription factor TFAP2A bound with the promotor region of SNHG16 and activated its transcription. In functional experiments, SNHG16 knockdown suppressed the proliferation, glycolysis and tumor growth of ECa cells. In mechanical experiments, SNHG16 upregulated HK2, the target gene of miR-490-3p, by competitively sponging miR-490-3p and then promoted endometrial carcinoma proliferation and glycolysis. In conclusion, this finding illustrates the vital role of SNHG16 via the TFAP2A/SNHG16/miR-490-3p/HK2 axis in the ECa proliferation and glycolysis, providing an interesting insight for the ECa tumorigenesis.