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Modulation of cell cycle‐related protein expression by sodium butyrate in human non‐small cell lung cancer cell lines
Author(s) -
Pellizzaro Cinzia,
Coradini Danila,
Daniotti Antonella,
Abolafio Gabriella,
Daidone Maria Grazia
Publication year - 2001
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 - 10.1002/1097-0215(200002)9999:9999<::aid-ijc1117>3.0.co;2-i
Subject(s) - sodium butyrate , cell cycle , biology , cyclin d1 , cell growth , retinoblastoma protein , butyrate , cell culture , cell , cancer research , cyclin , medicine , microbiology and biotechnology , biochemistry , genetics , fermentation
To elucidate the mechanism of action of sodium butyrate (NaB), we examined its effect on the expression of some cell cycle‐related proteins (cyclins D1 and E, p16 ink4 , p21 waf1 , p27 kip1 ) in 2 human non‐small cell lung cancer cell lines (NCI‐460 and NCI‐H23) characterized by wild‐ type and mutant TP53, respectively. The growth of both cell lines was inhibited in a dose‐dependent manner and this process was accompanied by a modulation of cell cycle‐related proteins. In NCI‐H460, the p27 kip1 and p16 ink4 protein levels were markedly increased following NaB treatment, whereas p21 waf1 was only slightly elevated, with a peak at 2 mM NaB, and p53 was unaffected by any concentration. By contrast, in NCI‐H23, a marked increase in p21 waf1 protein was paralleled by decreased p53 levels, whereas all the other investigated proteins remained stable. The results suggest that NaB blocks the growth of both cell lines by induction of cyclin‐dependent kinase inhibitors (in particular, p21 waf1 in NCI‐H23 and p27 kip1 and p16 ink4 in NCI‐H460) through a p53‐dependent or p53‐independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non‐small cell lung carcinoma. © 2001 Wiley‐Liss, Inc.