lncRNA PEG10 promotes cell survival, invasion and migration by sponging miR-134 in human bladder cancer.

Bladder cancer is one of common malignancies worldwide. lncRNAs and miRs are reported to play crucial roles in bladder cancer. We aimed to reveal the roles and mechanisms of lncRNA PEG10 and miR-134 in bladder cancer. Transfection was used to alter PEG10, miR-134, and LRP6 expression in human bladder cancer cell lines (T24 and HT1197). Then PEG10, miR-134 and LRP6 in cells as well as tissues were analyzed by qRT-PCR. The binding effect between miR-134 and PEG10 or LRP6 was detected by luciferase reporter assay. Viability, migration, invasion and apoptosis were evaluated by CCK-8, transwell assays and flow cytometry, respectively. LRP6 and factors related with apoptosis and signal pathways (Wnt/β-catenin and JAK/ATAT) were detected by Western blot. Finally, we established xenograft model and tumor volume and weight were both measured and weighted. We found the abnormal expression of PEG10, miR-134 and LRP6 in urinary bladder tissues and bladder cancer cell lines. PEG10 overexpression promoted viability, migration and invasion of T24 and HT1197 cells as well as facilitated tumor growth. PEG10 silence inhibited viability, migration and invasion, and induced apoptosis of T24 cells by upregulating miR-134 expression. PEG10 negatively regulated miR-134 expression. miR-134 targeted LRP6 and downregulated its expression. LRP6 promoted survival, migration and invasion of T24 cells and activated Wnt/β-catenin and JAK/STAT signal pathways. lncRNA PEG10 functioned as an oncogene in bladder cancer by sponging miR-134 and thus preventing LRP6 from degradation by miR-134. LRP6 promoted bladder cancer progression probably through activating Wnt/β-catenin and JAK/STAT signal pathways.