Fatostatin inhibits the insulin-induced adipogenesis of 3T3-L1 cells and the serum-independent growth of human androgen-independent prostate cancer (DU145) cells. Fatostatin blocks the activation of SREBPs in cells in tissue culture. Fatostatin suppresses cell proliferation and anchorage-independent colony formation in both androgen-responsive LNCaP and androgen-insensitive C4-2B prostate cancer cells. Fatostatin also reduced in vitro invasion and migration in both cell lines. Further, fatostatin causes G2/M cell cycle arrest and induces apoptosis by increasing caspase-3/7 activity and the cleavages of caspase-3 and PARP.
In vivo
Fatostatin blocks increases in body weight, blood glucose, and hepatic fat accumulation in obese ob/ob mice, even under uncontrolled food intake. Fatostatin significantly inhibits subcutaneous C4-2B tumor growth and markedly decreases serum PSA level compared to the control group.
