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Sulindac sulfide alters the expression of cyclin proteins in HT‐29 colon adenocarcinoma cells
Author(s) -
Qiao Liang,
Shiff Steven J.,
Rigas Basil
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19980330)76:1<99::aid-ijc16>3.0.co;2-b
Subject(s) - cyclin , cell cycle , sulindac , cyclin d1 , cyclin a , cyclin d , cancer research , cell growth , cyclin e , chemistry , cyclin b1 , cyclin d3 , cyclin b , biology , microbiology and biotechnology , cyclin dependent kinase 1 , apoptosis , biochemistry , pharmacology , nonsteroidal
Sulindac sulfide (SS), the active metabolite of the colon cancer chemopreventive compound sulindac, inhibits the proliferation of HT‐29 colon cancer cells mainly by inducing cell quiescence. We determined by bivariate flow‐cytometric analysis both the DNA and cyclin protein content of individual cells. Thus, we assessed in detail the expression of several cyclins during the cell‐cycle phases and demonstrated that SS (i) decreases the expression of cyclins B1 and E and (ii) increases the expression of cyclins D1, D2 and D3, particularly in the G 1 phase of the cell cycle. SS‐induced apoptotic cells expressed both E‐ and D‐type cyclins but not cyclin B1. The changes in cyclin expression combined with reduced catalytic activity of cyclin‐dependent kinases could explain in molecular terms the anti‐proliferative effect of SS on HT‐29 colon cancer cells. These changes may contribute to the chemopreventive effect of sulindac. Int. J. Cancer 76:99–104, 1998.© 1998 Wiley‐Liss, Inc.