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Tumor Progression and Metastasis Program [S. A., P. N-M., H. I., A. R.], Karmanos Cancer Institute, and Departments of Pathology [H-R. C. K.] and Radiation Oncology, Wayne State University School of Medicine [A. R.], Detroit, Michigan 48201
Galectin-3, a ß-galactoside-binding protein, has been shown to be involved in tumor progression and metastasis. Here, we demonstrate that expression of galectin-3 in human breast carcinoma BT549 cells inhibits cis-diamminedichloroplatinum (cisplatin)-induced poly(ADP-ribose) polymerase degradation and apoptosis, without altering Bcl-2, Bcl-XL, or Bax expressions. Galectin-3 contains the NWGR amino acid sequence highly conserved in the BH1 domain of the bcl-2 gene family, and a substitution of glycine to alanine in this motif abrogated its antiapoptotic activity. Our findings demonstrate that galectin-3 inhibits apoptosis through a cysteine protease pathway and highlight the functional significance of the NWGR motif in apoptosis resistance of a non-Bcl-2 protein.
1 This work was supported in part by United States Army Grant DAMD 17-96-1-6181, NIH Grants R29-CA64139 (to H-R. C. K.) and R01-CA46120 (to A. R.), The Henry Ford Health Sciences Center and NIH Grant R01-CA69480 (to A. R.), and the Paul Zuckerman Support Foundation for Cancer Research (to A. R.).
2 Present address: Department of Otolaryngology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan.
3 To whom requests for reprints should be addressed, at Tumor Progression and Metastasis, Karmanos Cancer Institute, 110 East Warren Avenue, Detroit, MI 48201. Phone: (313) 833-0960; Fax: (313) 831-7518.
Received 8/28/97. Accepted 10/16/97.
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