Methyltransferase like 13 promotes malignant behaviors of bladder cancer cells through targeting PI3K/ATK signaling pathway.

Abstract

Bladder cancer (BC) is the tenth most common tumor worldwide, characterized by high incidence rates and mortality. This study aimed to explore the role of Methyltransferase like 13 (METTL13) in BC cells. J82 and T24 cells were cultured for in vitro experiments. Cell viability, migration, and invasion were assessed using CCK-8 and transwell assays. Senescence-associated beta-galactosidase (SA-β-gal) levels were detected using a β-galactosidase staining kit. METTL13 and cell cycle-related protein levels were quantified using RT-qPCR and Western blotting. The results showed that METTL13 was upregulated in BC cells. Silencing METTL13 decreased cell viability, migration, and invasion in BC cells, whereas METTL13 overexpression increased these parameters. Additionally, METTL13 knockdown inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Inhibition of the PI3K/AKT pathway reversed the effects of METTL13 on cell viability, migration, invasion, and cell cycle-related proteins in BC cells. In vivo experiments showed that METTL13 knockdown inhibited tumor growth and development. In conclusion, this study demonstrated that METTL13 promoted the malignant behaviors of BC cells through activation of the PI3K/AKT signaling pathway. METTL13 may be a promising therapeutic target for BC in the future.