ArticleWorld journal of gastroenterology2003
Synergistic effect of cell differential agent-II and arsenic trioxide on induction of cell cycle arrest and apoptosis in hepatoma cells.
Article in World journal of gastroenterology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Protective role of metallothionein (I/II) against pathological damage and apoptosis induced by dimethylarsinic acid.World journal of gastroenterology · 2004Article
- Experimental study on therapeutic effect of in vivo expression of Cell I-Hep II recombinant polypeptide of fibronectin on murine H22 hepatocellular carcinoma.World journal of gastroenterology · 2003Article
- Effects of hydroxyapatite nanoparticles on proliferation and apoptosis of human hepatoma BEL-7402 cells.World journal of gastroenterology · 2003Article
- Isolation of a novel member of small G protein superfamily and its expression in colon cancer.World journal of gastroenterology · 2003Article
- Gene-expression analysis of single cells-nested polymerase chain reaction after laser microdissection.World journal of gastroenterology · 2003Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo illustrate the possible role of cell differential agent-II (CDA-II) in the apoptosis of hepatoma cells induced by arsenic trioxide (As(2)O(3)).
methodsHepatoma cell lines BEL-7402 and HepG2 were treated with As(2)O(3) together with CDA-II. Cell surviving fraction was determined by MTT assay; morphological changes were observed by immunofluorescence staining of Hoechst 33,258; and cell cycle and the apoptosis index were determined by flow cytometry (FCM).
resultsCytotoxicity of CDA-II was low. Nevertheless, CDA-II could strongly potentiate arsenic trioxide-induced apoptosis. At 1.0 g/L CDA-II, IC(50) of As(2)O(3) in hepatoma cell lines was reduced from 5.0 micromol/L to 1.0 micromol/L (P<0.01). The potentiation of apoptosis was dependent on the dosage of CDA-II. FCM indicated that in hepatoma, cell growth was inhibited by CDA-II at lower concentrations (<2.0 g/L) primarily by arresting at S and G(2) phase, and at higher concentrations (>2.0 g/L) apoptotic cell and cell cycle arresting at G(1) phase increased proportionally. The combination of two drugs led to much higher apoptotic rates, as compared with the either drug used alone.
conclusionCDA-II can strongly potentiate As(2)O(3)-induced apoptosis in hepatoma cells, and two drugs can produce a significant synergic effect.
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