Roles of JNK‐1 and p38 in selective induction of apoptosis by capsaicin in ras‐transformed human breast epithelial cells

摘要: Efforts have been made to develop a chemoprevention strategy that selectively triggers apoptosis in malignant cancer cells. Previous studies showed capsaicin, the major pungent ingredient of red pepper, had differential effect between normal and transformed As an approach unveil molecular mechanism by which capsaicin induces cells, we investigated nontransformed ras-transformed cells common origin: parental (MCF10A) H-ras-transformed (H-ras MCF10A) human breast epithelial Here, show but not their cell counterparts. The capsaicin-induced apoptosis, is dependent on ras transformation, involves activity DEVDase (caspase-3 like). In H-ras MCF10A treatment markedly activated c-Jun N-terminal protein kinase (JNK)-1 p38 matigen-activated (MAPK) while it deactivated extracellular signal-regulated kinases (ERKs). use inhibitors overexpression dominant-negative forms MAPKs demonstrated role JNK-1 p38, ERKs, induced Based present study, propose through modulation ras-downstream signaling molecules ras-activated Taken conjunction with fact uncontrolled activation probably most genetic defect our finding may be critical chemopreventive potential for developing induce tumor cell-specific apoptosis.