c-Jun is involved in interstitial cystitis antiproliferative factor (APF)-induced growth inhibition of human bladder cancer T24 cells

AbstractObjective over the role of c-Jun, a proto-oncogene, in inhibitory effects of antiproliferative factor (APF) on tumor cell growth. als and Methods sion of c-Jun was analyzed by Western blotting in 45 clinical specimens (30 tumorous tissues and 15 paired non-tumorous tissues) and 3 bladder cancer cell lines. APF-responsive T24 transitional carcinoma bladder cells were treated with APF or mock control. Cell proliferation was measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. Change of c-Jun expression was detected by RT-PCR and Western blotting. The influence of c-Jun on APF treatment was evaluated by transient transfection of c-Jun and MTT assay in T24 cells. s was significantly higher in invasive bladder cancer tissues and cell lines. T24 cells treated with APF had decreased c-Jun expression and suppressed cell growth. More importantly, ectopic c-Jun attenuated APF inhibitory effects on cell growth. sions observations suggest that c-Jun is involved in APF-mediated inhibition for bladder tumor cell growth, as potential target of APF in patients with aggressive bladder carcinoma.