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Cell Growth & Differentiation Vol. 11, 1-10, January 2000
© 2000 American Association for Cancer Research


Articles

Selective Loss of the Transforming Growth Factor-ß Apoptotic Signaling Pathway in Mutant NRP-154 Rat Prostatic Epithelial Cells1

Sarit Larisch-Bloch, David Danielpour, Nanette S. Roche, Rona Lotan, Andrew Y. Hsing, Hedviga Kerner, Taleb Hajouj, Robert J. Lechleider2 and Anita B. Roberts3

Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892-5055 [S. L-B., N. S. R., A. Y. H., R. J. L., A. B. R.]; Department of Pathology, Rambam Medical Center, Haifa 31096, Israel [S. L-B., R. L., H. K., T. H.]; Cancer Center and Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio 44106 [D. D.]

Abstract

Retroviral insertional mutagenesis was used to select mutant NRP-154 rat prostate carcinoma cells resistant to transforming growth factor (TGF)-ß-induced cell death. Similar to the parental cells, a mutant clone, M-NRP1, expressed TGF-ß receptors and was still responsive to induction both of direct target genes by TGF-ß and of apoptosis by staurosporine or okadaic acid. In contrast, indicators of cell growth, strongly suppressed by TGF-ß in the parental cells, were unaffected in M-NRP1 cells. M-NRP1 cells overexpress the antiapoptotic protein, Bcl-xL, and show dysregulated expression and localization of a protein related to a novel human septin, ARTS (designation of apoptotic response to TGF-ß signals), cloned by homology to an exonic sequence flanked by the viral long terminal repeats in M-NRP1 cells and shown to make cells competent to undergo apoptosis in response to TGF-ß. We propose that ARTS might operate within the same apoptotic pathway as Bcl-xL and that M-NRP1 cells could serve as a useful model for characterization of this pathway.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 2000 by the American Association of Cancer Research.