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. 2013 Feb;31(2):228-33.
doi: 10.1016/j.urolonc.2010.11.011. Epub 2011 Aug 26.

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

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

Zeliang Li et al. Urol Oncol. 2013 Feb.

Abstract

Objective: To uncover the role of c-Jun, a proto-oncogene, in inhibitory effects of antiproliferative factor (APF) on tumor cell growth.

Materials and methods: Expression 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.

Results: c-Jun 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.

Conclusions: These 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.

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