Abstract:
:The mechanism underlying the chemopreventive effects of the non-steroidal anti-inflammatory drug sulindac remains unclear. Its active metabolite, sulindac sulfide, induces cell cycle arrest as well as apoptosis in mammalian cell lines. We now show that in murine thymocytes, sulindac sulfide-induced cell death is p53, bax, Fas, and FasL independent. In contrast, bcl2 transgenic thymocytes are resistant to sulindac sulfide-induced apoptosis. In addition, we demonstrate that sulindac sulfide-induced cell cycle arrest in mouse embryonic fibroblasts (MEFs) is partly mediated by the retinoblastoma tumor suppressor protein (Rb) and the cyclin kinase inhibitor p21waf1/cip1. Furthermore, MEFs deficient in p21 or Rb are more susceptible to sulindac sulfide-induced cell death. These results suggest that sulindac may selectively target premalignant cells with cell cycle checkpoint deficits.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Jung B,Barbier V,Brickner H,Welsh J,Fotedar A,McClelland Mdoi
10.1016/j.canlet.2004.06.015keywords:
subject
Has Abstractpub_date
2005-02-28 00:00:00pages
15-25issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(04)00460-4journal_volume
219pub_type
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