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Dominant Nature of the Resistance to Fas- and Tumor Necrosis Factor--mediated Apoptosis in Human Prostatic Carcinoma Cell Lines¹

Departments of Pathology [O. W. R., R. A. G., M. B. C.], Microbiology [B. S. H., G. A. B.], and Urology [M. B. C.], University of Iowa, Iowa City, Iowa 52242; Institute of Experimental Pathology, Oncology and Radiobiology, Kiev, Ukraine, 252022 [S. P. S.]; and Department of Genetics, University of Illinois at Chicago, Chicago, Illinois 60607 [A. V. G.]

We have recently found (O. W. Rokhlin et al., Cancer Res., 57: 1758–1768, 1997) that, although Fas ligation induced apoptosis in two of six human prostatic carcinoma cell lines investigated, the apoptotic machinery involved in Fas-mediated killing is already in place in Fas-resistant cell lines. Here, we investigated Fas- and tumor necrosis factor- (TNF-)-mediated apoptosis in cell hybrids between resistant (DU145 and JCA1) and sensitive (ALVA31 and PC3) cell lines. All three types of hybrid cells investigated, F1(DU145 x PC3), F1(JCA1 x PC3), and F1(JCA1 x ALVA31), were found to be resistant to Fas- and TNF--mediated apoptosis at the same level as the corresponding parental resistant cell lines. These results indicate that resistance to Fas- and TNF--mediated apoptosis dominates over sensitivity in cell hybrids and suggest that resistance may be regulated by an apoptosis suppressor factor or factors acting in resistant but not in sensitive cells.

¹ This work was supported by National Aeronautics and Space Administration Grant NAG9-824 and a Veterans Affairs Merit Award (to M. B. C.); NIH Grants A128847 and CA66570 (to G. A. B.); NIH Postdoctoral Training Grant T32AI07260 (to B. S. H.); and NIH Grants RO1CA60730 and RO1CA75179 (to A. V. G.). S. P. S. is a Howard Hughes Medical Institute International Research Scholar.

² To whom requests for reprints should be addressed, at Department of Pathology, 118 ML, University of Iowa Hospital and Clinics, Iowa City, IA 52242. Phone: (319) 335-8214; Fax: (319) 335-8348.

Received 7/ 2/97. Accepted 7/31/97.

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