Long non-coding RNA MEG3 functions as a competing endogenous RNA of miR-93 to regulate bladder cancer progression via PI3K/AKT/mTOR pathway.

BACKGROUND

Maternally expressed gene 3 () is a long non-coding RNA (lncRNA) and involved in progression of various human tumors. However, its underlying regulatory mechanism in tumorigenesis of bladder cancer (BC) remains unclear. To demonstrate effects of on BC cell proliferation and elaborate its regulatory mechanism in BC.

METHODS

Aberrant expressions of and were induced by cell transfection. The mRNA and protein expression were analyzed using qRT-PCR and western blot. Cell proliferation was examined by CCK-8 assay and EdU staining. The targeted regulation effect of on was confirmed by luciferase reporter assay. The number of LC3 punctated cells was detected by immunofluorescence. Xeno-graft mouse model was constructed for validation.

RESULTS

was down-regulated with increased expression of in BC cells and tissues. Luciferase reporter assay showed that was a direct target of and was negatively regulated by . overexpression inhibited cell proliferation and the expression of proliferation-, apoptosis- and autophagy-related proteins. The activation of PI3K/AKT/mTOR pathway was also suppressed with elevated cell apoptosis. overexpression counteracted these results. experiments, we confirmed that overexpression reversed the overexpression-mediated suppression on tumor growth and protein expression.

CONCLUSIONS

lncRNA could function as a competing endogenous RNA of to regulate the tumorigenesis of BC via PI3K/AKT/mTOR pathway. The present research provided a new perspective to understanding the pathogenic mechanism of BC, and an effective therapeutic target for BC.