TGFß1 induces apoptosis in invasive prostate cancer and bladder cancer cells via Akt-independent, p38 MAPK and JNK/SAPK-mediated activation of caspases.

Recent findings indicate that advanced stage cancers shun the tumor suppressive actions of TGFß and inexplicably utilize the cytokine as a tumor promoter. We investigated the effect of TGFß1 on the survival and proliferation of invasive prostate (PC3) and bladder (T24) cancer cells. Our study indicated that TGFß1 decreased cell viability and induced apoptosis in invasive human PC3 and T24 cells via activation of p38 MAPK-JNK-Caspase9/8/3 pathway. Surprisingly, no change in the phosphorylation of pro-survival Akt kinase was observed. We postulate that TGFß1 pathway may be utilized for specifically targeting urological cancers without inflicting side effects on normal tissues.