Androgen receptor inducing bladder cancer progression by promoting an epithelial-mesenchymal transition.

The study investigated the role of androgen receptor (AR) as a potential target for the treatment of bladder cancer in regulating epithelial-mesenchymal transition or transformation (EMT). Cell proliferation, and migration capacity were determined in bladder cancer T24 cells treated with small interfering RNA directed against AR, and expression levels of E-cadherin, β-catenin and N- cadherin were assessed using quantitative reverse transcription PCR (qRT-PCR). Tumour cell growth was evaluated in vivo in T24 tumour-bearing nude mice receiving electroporation-assisted administration of anti-AR small interfering RNA. It was found that low AR expression decreased proliferation and migration of bladder cancer cells. In vivo experiments showed that silencing AR expression significantly suppressed AR-positive bladder tumour growth with decreased cell proliferation. Low AR level of T24 bladder cancer cells treated with dehydrotestosterone (DHT) decreased expression of E-cadherin, β-catenin and N-cadherin expression, indicating a strong sensitivity to the EMT and In cells with low AR content, TGF-β induced down-regulation of E-cadherin and β-catenin. It is concluded that suppression of AR expression decreased the production of TGF-β, inhibiting EMT and bladder cancer cell growth in vitro and in vivo, implying that its use might be a potential therapeutic target for the treatment of bladder cancer.