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Isatis indigotica induces hepatoma cell apoptosis via caspase‐independent pathway in vitro and in vivo
Author(s) -
Chiang EnPei Isabel,
Chung YingChun,
Tang FengYao,
Chung ChiaHua
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.720.11
Subject(s) - apoptosis , in vivo , in vitro , chemistry , carcinogenesis , cell growth , cell culture , cell cycle checkpoint , caspase 3 , cell , programmed cell death , cancer research , cell cycle , microbiology and biotechnology , biology , biochemistry , genetics , gene
We explored the chemotherapeutic potential of an Asian biennial herbaceous Cruciferae Isatis indigotica and investigated the mechanism by which it inhibits tumor growth in vitro and in vivo. Chloroform extract from dried leafs (CEDLI) had the strongest anti‐tumor activity among all fractions examined. CEDLI supplementation (0.26% for 2 mo) inhibited pre‐developed xenografted hepatoma growth by 43 % without inducing toxicity. Tumor immunohistochemical analysis showed a 33% decrease in proliferation and a 3.6‐fold increase in cell apoptosis in vivo. CEDLI induced sub‐G1 cell cycle arrest and apoptosis by activating p53, inducing Bax and reducing Bcl‐2, which in turn caused mitochondrial stress and led to the release of mitochondrial apoptosis inducing factor into the cytosol, followed by its translocation into the nuclear, resulting apoptosis in hepatoma cell‐lines. We provide novel in vivo evidence that Isatis indigotica has antitumor activity against liver tumorigenesis, and the chemotherapeutic activity of Isatis indigotica on hepatoma was associated with a distinguished caspase‐independent apoptotic pathway. Results from this study provide the molecular basis for Isatis indigotica as a potential anticancer treatment against human hepatoma.