Armstrong D K, Kaufmann S H, Ottaviano Y L, Furuya Y, Buckley J A, Isaacs J T, Davidson N E
Johns Hopkins Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287.
Cancer Res. 1994 Oct 15;54(20):5280-3.
MDA-MB-468 human breast cancer cells lack estrogen receptors, overexpress epidermal growth factor (EGF) receptors, and are growth inhibited by EGF. We show that treatment of MDA-MB-468 cells with EGF leads to inhibition of cell proliferation, fragmentation of DNA into nucleosomal oligomers, and the development of apoptotic morphology. This treatment is associated with increased expression of c-myc, c-fos, jun family members, and transforming growth factor beta 1 mRNA and with partial proteolytic cleavage of poly(ADP-ribose) polymerase and lamin B. The observation that EGF can mediate apoptosis in EGF receptor-overexpressing cells has important implications for clinical efforts directed at the EGF receptor.
