Document Detail

Loss of butyrate-induced apoptosis in human hepatoma cell lines HCC-M and HCC-T having substantial Bcl-2 expression.
MedLine Citation:
PMID:  9581676     Owner:  NLM     Status:  MEDLINE    
We have demonstrated that sodium butyrate induces differentiation in human hepatoma cells; however, recent studies have shown that this agent causes apoptosis in some types of cancer cells. In this study, we examined whether sodium butyrate causes apoptosis in the human hepatoma cell lines, HCC-M and HCC-T. The growth of human hepatoma cells was dose-dependently reduced by sodium butyrate. Flow cytometric analysis showed cell-cycle arrest at the G1 phase in the sodium butyrate-treated cells. Apoptotic change was never found in treated cells at concentration levels of less than 5 mmol/L. Sodium butyrate decreased p53 expression and increased p21WAF-1 expression in HCC-T and HCC-M cells having the wild-type p53 gene. Western blot analysis showed that Bcl-2 was expressed in the HCC-T and HCC-M cells, and its expression was increased after exposure to sodium butyrate. Antisense oligodeoxynucleotide against bcl-2 easily caused apoptosis. These results indicate that sodium butyrate hardly induces apoptotic change in the human hepatoma cell lines, HCC-T and HCC-M, with the increase of Bcl-2 expression. Cell-cycle arrest in the G1 phase caused by sodium butyrate was suggested to be induced by the increase in p21WAF-1 expression, but this change did not link with the p53 increase.
H Saito; H Ebinuma; M Takahashi; F Kaneko; K Wakabayashi; M Nakamura; H Ishii
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  27     ISSN:  0270-9139     ISO Abbreviation:  Hepatology     Publication Date:  1998 May 
Date Detail:
Created Date:  1998-05-19     Completed Date:  1998-05-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1233-40     Citation Subset:  IM    
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
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MeSH Terms
Apoptosis / drug effects*
Blotting, Western
Butyrates / pharmacology*
Carcinoma, Hepatocellular / pathology*
Cell Cycle / drug effects
Cell Division / drug effects
Cyclin-Dependent Kinase Inhibitor p21
Cyclins / metabolism
Genes, p53
Neoplasm Proteins / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism*
Tumor Cells, Cultured
Tumor Suppressor Protein p53 / metabolism
Reg. No./Substance:
0/Butyrates; 0/CDKN1A protein, human; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Neoplasm Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Suppressor Protein p53

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