Abstract
MDA-MB-468 human breast cancer cells lack estrogen receptors, over-express 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 β1 mRNA and with partial proteolytic cleavage of poly(ADP-ribose) polymerase and lamin B. The observation that EGF can mediate apoptosis in EGF receptor-over-expressing cells has important implications for clinical efforts directed at the EGF receptor.
Footnotes
-
↵1 These studies have been supported by NIH Grant CA 57545 (to N. E. D.) and the Susan G. Komen Foundation (to D. K. A.). S. H. K. is a Leukemia Society Scholar.
-
↵2 To whom requests for reprints should be addressed, at Johns Hopkins Oncology Center, 422 N. Bond Street, Baltimore, MD 21231.
- Received July 15, 1994.
- Accepted August 23, 1994.
- ©1994 American Association for Cancer Research.
Volume 54, Issue 20
