Abstract
Long noncoding RNA paternally expressed gene 10 (lncRNA PEG10) has been certified to regulate cell proliferation, metastasis, and apoptosis in diversified cancer cells. Nevertheless, the functions of PEG10 in bladder cancer cells remain uninvestigated. We tried to probe the impacts of PEG10 on proliferation, migration, and invasion of bladder cancer cells. PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/β-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/β-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-29b-Wnt/β-catenin-JNK axis.