The expression levels of ALKBH3 protein in the urothelial cell carcinoma and para-carcinoma tissues， normal bladder epithelial cells （SV-HRUC-1）， and bladder cancer cells （BIU87 and T24） were detected by immunohistochemistry and Western blotting method， respectively. The BIU87 and T24 cells were divided into sh-Con group （transfected with sh-Con） and sh-ALKBH3 group （transfected with sh-ALKBH3）. The cell viabilities and the number of colony， migration and invasion in two groups were detected by CCK-8 method， colony formation experiment and Transwell chamber assay， respectively. The number of migration cells and the tubule formation rate of human umbilical vein endothelial cells （HUVEC） induced by cell culture medium in two groups were detected by Transwell chamber and tubule formation assays， respectively. After the xenograft tumor model was constructed， the tumor volumes in two groups were measured regularly with vernier caliper， and the expression levels of CD31 protein in the tumor tissue in two groups were detected by immunohistochemistry. The expression levels of vascular endothelial growth factor-A（VEGF-A） protein in invivo and invitro experiments intwo groups were detected by Western blotting method.

Compared with para-carcinoma tissue or SV-HRUC-1 cells， the expression levels of ALKBH3 proteins in urothelial cell carcinoma tissue and bladder cancer cells （BIU87 and T24） were significantly increased （P<0.01）. The invitro experiment results showed that compared with sh-Con group， the cell activities， the number of migration and invasion BIU87 and T24 cells， as well as the number of induced migration HUVEC and the tubule formation rate of HUVEC in sh-ALKBH3 group were significantly decreased （P<0.01）. The vivo experiment results showed that compared with sh-Con group， the tumor volume in sh-ALKBH3 group was significantly reduced， and the expression level of CD31 protein in tumor tissue was significantly decreased （P<0.01）. Compared with sh-Con group， the expression levels of VEGF-A protein in invivo and in vitro experiments in sh-ALKBH3 group were significantly decreased （P<0.01）.

ALKBH3 knockdown contributes to inhibiting the growth， migration， invasion and tumor angiogenesis of bladder cancer cells， and its mechanism may be related to the down-regulation of VEGF-A expression.