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Apigenin and naringenin decrease cell number in a dose dependent manner in non‐transformed young adult mouse colonocytes (YAMC) but not in those expressing a dominant negative p53‐mutant (mp53 YAMC)
Author(s) -
Daniels Wesley Danielle,
Allred Kimberly F.,
Allred Clinton D.,
Patil Bhimanagouda S.,
Turner Nancy D.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.639.7
Subject(s) - naringenin , apigenin , chemistry , apoptosis , cell growth , mutant , cell , cell culture , flavones , biochemistry , pharmacology , flavonoid , microbiology and biotechnology , biology , genetics , antioxidant , chromatography , gene
We have shown that apigenin and naringenin (flavonoids) suppress colon carcinogenesis by inducing apoptosis and suppressing proliferation in rats. The aim of this study was to determine if the mechanism of action was p53 dependent. YAMC and mp53 YAMC cells were treated with apigenin (0.1 μM, 1μM, 10 μM), naringenin (0.1 μM, 1 μM, 10 μM, 25 μM, 50 μM), or estradiol (1 nM, positive control) in DMSO for 4 d at non‐permissive conditions. Cells were counted and proliferation measured using Brd‐U. YAMC cells treated with 1 μM or greater apigenin or naringenin exhibited dose‐dependent decreases (P<0.005) in cell numbers compared to DMSO. No differences in cell number were identified in the mp53 YAMC cells except with the highest concentration of apigenin and naringenin (P < 0.0001). No differences in proliferation were observed with apigenin or naringenin in either cell line. The dose‐dependent reduction in non‐transformed cell number induced by apigenin and naringenin are in part p53‐mediated. The reduction of cell numbers in mp53 YAMC cells resulting from the greatest concentrations suggests alternate pathways can be induced by these flavonoids. However, the effect on cell number is not linked directly to suppression of colonocyte proliferation in either p53 competent or mutant colonocytes. Funded by USDA/VFIC 2010–34402‐20875.