Vitamin E succinate induces Fas-mediated apoptosis in estrogen receptor-negative
human breast cancer cells.
Turley JM, Fu T, Ruscetti FW, Mikovits JA, Bertolette DC 3rd, Birchenall-Roberts
MC.
Laboratory of Leukocyte Biology, Division of Basic Sciences, National Cancer
Institute, Frederick, Maryland 21702, USA.
"Vitamin E succinate (VES), a derivative of the fat-soluble vitamin
D-alpha-tocopherol (vitamin E), inhibited growth and induced apoptotic cell death
of estrogen receptor-negative human breast cancer cells. VES-induced apoptosis in
MDA-MB-231 and SKBR-3 cells occurred through a Fas pathway. Total protein levels
of the Fas receptor (Fas; APO-1/CD-95) and the Fas ligand (Fas-L) were increased
following VES treatment. In addition, VES increased cell surface Fas expression.
Fas-neutralizing antibodies and Fas-L antisense oligonucleotides blocked
VES-induced apoptosis. The presence of Fas-L antisense oligonucleotides also
completely blocked the VES-mediated increase in Fas-L protein expression. These
data indicate a role for Fas signaling in VES-mediated apoptotic cell death of
human breast cancer cells. These findings also suggest that VES may be of
clinical use in the treatment of aggressive human breast cancers, particularly
those that are refractory to antiestrogen therapy."
human breast cancer cells.
Turley JM, Fu T, Ruscetti FW, Mikovits JA, Bertolette DC 3rd, Birchenall-Roberts
MC.
Laboratory of Leukocyte Biology, Division of Basic Sciences, National Cancer
Institute, Frederick, Maryland 21702, USA.
"Vitamin E succinate (VES), a derivative of the fat-soluble vitamin
D-alpha-tocopherol (vitamin E), inhibited growth and induced apoptotic cell death
of estrogen receptor-negative human breast cancer cells. VES-induced apoptosis in
MDA-MB-231 and SKBR-3 cells occurred through a Fas pathway. Total protein levels
of the Fas receptor (Fas; APO-1/CD-95) and the Fas ligand (Fas-L) were increased
following VES treatment. In addition, VES increased cell surface Fas expression.
Fas-neutralizing antibodies and Fas-L antisense oligonucleotides blocked
VES-induced apoptosis. The presence of Fas-L antisense oligonucleotides also
completely blocked the VES-mediated increase in Fas-L protein expression. These
data indicate a role for Fas signaling in VES-mediated apoptotic cell death of
human breast cancer cells. These findings also suggest that VES may be of
clinical use in the treatment of aggressive human breast cancers, particularly
those that are refractory to antiestrogen therapy."