Up-Regulation of LINC00158 Contributes to Endometrial Carcinoma Progression by Interacting with HMGB2

Abstract

Background: Increasing evidence has reported lncRNAs exhibit significant biological functions in regulating endometrial carcinoma (EC) progression. LINC00158 has been identified as a crucial modulator in various diseases. Nevertheless, the specific molecular mechanism of LINC00158 in EC remains to be investigated.Methods:q-PCR and Western blot analysis were performed to determine the expression of LINC00158 and HMGB2 in EC tissues and cells. Cell viability assay, EdU assay, flow cytometry, wound healing assay and transwell invasion assay were used to evaluate their effects on EC cell proliferation, migration and invasion. RIP assay was used to verify the interactions between LINC00158 and HMGB2. Xenograft tumor model was established to confirm the effects of LINC00158 in vivo.Results:INC00158 was obviously up-regulated in EC tissues in comparison to the normal endometrium. LINC00158 was greatly increased in EC cells than in the immortalized endometrial fibroblast cell T-HESCs. Cell viability of EC cells was reduced as indicated using CCK-8 assay and EdU experiments by knockdown of LINC00158. Loss of LINC00158 obviously induced EC cell apoptosis and blocked cell cycle, repressed EC cell migration and invasion capacity. HMGB2 was remarkably increased in EC tissues and it was positively correlated with LINC00158 expression. RIP assay was carried out and confirmed the direct binding relationship between LINC00158 and HMGB2. Decrease of LINC00158 was able to reduced HMGB2 expression in AN3CA and HEC1-A cells. LINC00158 activated HMGB2 to promote EC progression in vivo.Conclusions: Our findings implied high expression of LINC00158 promoted EC progression via interacting with HMGB2.