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Fibroblast growth factor receptor 3 (FGFR3) is a high frequency mutant gene in bladder cancer (BCa) and has become a promising therapeutic target due to its involvement in cell proliferation and migration. However, whether and how FGFR3 mutations affects BCa cell chemosensitivity is unknown. The current study aimed to elucidate the role of the FGFR3 S249C mutation in the development of chemoresistance in BCa cells. The results revealed that 97-7 (FGFR3 S249C ) cells had decreased sensitivity to cisplatin compared with 5637 (FGFR3 WT ) and T24 (FGFR3 WT ) cells. The ratio of phosphorylated-Akt/total-Akt was higher in 97-7 (FGFR3 S249C ) cells, which was reversed by knockdown of FGFR3. Furthermore, inhibition of Akt signaling by GDC0068 or LY294002 increased the cisplatin sensitivity of 97-7 (FGFR3 S249C ) cells. GDC0068 or LY294002 was also revealed to augment the effects of cisplatin on 97-7 (FGFR3 S249C ) cell proliferation and apoptosis. The results of the present study demonstrated that the FGFR3 S249C mutation promotes chemoresistance in BCa cells by activating the Akt signaling pathway. The FGFR3 S249C mutation may therefore be used as a predictor of chemosensitivity in patients with BCa.

FGFR3S249C mutation promotes chemoresistance by activating Akt signaling in bladder cancer cells