Interon-gamma enhances the antitumor effect of all-trans retinoic acid on hepatocellular carcinoma cells by inhibiting the expression of nuclear factor-kappaB

Objective To explore the combination effects of all-trans retinoic acid (ATRA) with interferon-gamma (IFN-γ) on human hepatocarcinoma cell line SMMC-7721 and the mechanism of action. Methods SMMC-7721 cells were divided into treated group and control group. The cells were treated with ATRA or ATRA+...

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Published inChinese journal of cancer research Vol. 20; no. 3; pp. 211 - 215
Main Authors Yin, Yuan-qin, Wang, Xiao-hua, Ma, Ping, Fu, Li-ye, Jiang, Tao, Wang, Yang
Format Journal Article
LanguageEnglish
Published Heidelberg Chinese Anti-Cancer Association 01.09.2008
Cancer Institute,the First Affiliated Hospital,China Medical University,Shenyang 110001,China
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Summary:Objective To explore the combination effects of all-trans retinoic acid (ATRA) with interferon-gamma (IFN-γ) on human hepatocarcinoma cell line SMMC-7721 and the mechanism of action. Methods SMMC-7721 cells were divided into treated group and control group. The cells were treated with ATRA or ATRA+ IFN-γ in the former and added with PBS in the latter. The inhibition rate of SMMC-7721 cell proliferation was detected by MTT, the cell change in morphology was observed by electron microscope. The apoptosis was detected by flow cytometry and the expression changes of nuclear factor-kappaB (NF-κB) was analyzed by Western blotting when the SMMC-7721 cells were treated with ATRA and IFN-γ. Results The SMMC-7721 cell proliferation was suppressed and apoptosis was induced after the cells were treated with ATRA treatment, and these effects were enhanced when ATRA was combined with IFN-γ. The expression of NF-κB was reduced after SMMC-7721 cell was treated with ATRA, and reduced significantly when the cells were treated with the combination of ATRA and IFN-γ. Conclusion IFN-γ can enhance the inhibiting effects of ATRA on cell proliferation and inducing apoptosis on SMMC-7721 cell and these effects might be mediated by inhibiting the expression of NF-κB.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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content type line 23
ISSN:1000-9604
1993-0631
DOI:10.1007/S11670-008-0211-0