ArticleAnnals of surgery1998
Effects of 5-azacytidine and butyrate on differentiation and apoptosis of hepatic cancer cell lines.
Article in Annals of surgery, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 43 citations in OpenAlex.
- Microbiota-derived metabolites in tumorigenesis: mechanistic insights and therapeutic implications.Frontiers in pharmacology · 2025Review
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- Cancer Stem Cells: Dynamic Entities in an Ever-Evolving Paradigm.Biology and medicine (Aligarh) · 2015Article
- 5-Azacytidine enhances the radiosensitivity of CNE2 and SUNE1 cells in vitro and in vivo possibly by altering DNA methylation.PloS one · 2014Article
- Advantages of assessing lipoprotein profiles in hepatic cell differentiation.In vitro cellular & developmental biology. Animal · 2013Article
- Butyrate induces sLex synthesis by stimulation of selective glycosyltransferase genes.Biochemical and biophysical research communications · 2007Article
- Cytotoxicity of psammaplin A from a two-sponge association may correlate with the inhibition of DNA replication.BMC cancer · 2004Article
- Mechanisms of 5-azacytidine (5AzC)-induced toxicity in the rat foetal brain.International journal of experimental pathology · 2002Article
- Activation of conventional PKC isoforms increases expression of the pro-apoptotic protein Bad and TRAIL receptors.International journal of gastrointestinal cancer · 2002Article
- Effect of 5-azacytidine and galectin-1 on growth and differentiation of the human b lymphoma cell line bl36.Cancer cell international · 2001Article
- Significant augmentation of pro-apoptotic gene therapy by pharmacologic bcl-xl down-regulation in mesothelioma.Cancer gene therapy · 2001Article
- Expression of regulating apoptosis gene and apoptosis index in primary liver cancer.World journal of gastroenterology · 2000Article
- Effect of arsenic trioxide on human hepatoma cell line BEL-7402 cultured in vitro.World journal of gastroenterology · 2000Article
- Sodium butyrate modulates cell cycle-related proteins in HT29 human colonic adenocarcinoma cells.Cell proliferation · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo determine the cellular effects of 5-azacytidine (5-azaC) and sodium butyrate on two human liver cancers, HepG2 and Hep3B. SUMMARY BACKGROUND DATA: Primary liver cancer is a significant health problem; treatment options are limited and prognosis is poor. Recent studies have focused on the role that programmed cell death (i.e., apoptosis) plays in both normal and neoplastic growth: certain genes can either suppress (e.g., Bcl-2, Bcl-xL) or promote (e.g., Bik, Bax, Bak) apoptosis. The identification of novel agents targeted to specific molecular pathways may be beneficial in the treatment of this disease.
methodsHuman liver cancer cell lines HepG2 and Hep3B were treated with 5-azaC alone, butyrate alone, or 5-azaC and butyrate. Morphologic and proliferative changes were assessed by light microscopy and 5-bromo-2'-deoxyuridine staining; flow cytometry was used to determine cell cycle characteristics. Apoptosis was assessed by DNA laddering and the in situ apoptosis detection assay using the TdT-mediated dUTP nick end labeling method. In addition, total RNA and protein were analyzed by ribonuclease protection and Western blot, respectively, to assess changes in the expression of apoptosis-related genes.
resultsTreatment with either 5-azaC or butyrate inhibited cell growth and induced apoptosis in both HepG2 and Hep3B cells; the combination of 5-azaC and butyrate was not more effective than either agent alone. 5-azaC alone resulted in a more differentiated-appearing morphology and G2 cell cycle arrest in both cell lines. Treatment with 5-azaC or butyrate affected the expression levels of proteins of the Bcl-2 family.
conclusionsBoth 5-azaC and butyrate induced apoptosis in the HepG2 and Hep3B liver cancer cells; 5-azaC treatment alone produced G2 arrest in both cell lines. Proteins of the Bcl-2 family may play a role in the cellular changes that occur with treatment, but further studies are required to define this potential role. Products of the apoptotic pathway may prove to be useful therapeutic targets in the treatment of hepatic cancers.
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