Original Article
In vitro and in vivo suppression of hepatocellular carcinoma by Amorphophallus konjac tuber through regulation of survivin and bax
Abstract
Background: Amorphophallus konjac tuber (AKT) is used in traditional Chinese medicine (TCM) to treat various types of cancer. Our study aims to evaluate the antitumor activity of AKT against hepatocellular carcinoma both in vitro and in vivo, as well as the underlying mechanisms.
Methods: AKT was extracted by aqua and organic solutions. The antitumor activity of the organic extract was tested in hepatocellular carcinoma cell lines Huh7 and H22, the latter was also used to establish mouse tumor model. Cell apoptotic rate was analyzed by flow cytometry. In vivo expression of apoptosis associated proteins survivin and bax were analyzed by immunohistochemistry (IHC).
Results: AKT exhibited antitumor activity against hepatocellular carcinoma cell lines. In vivo suppression of H22 was comparable with 5-fluorouracil (5-FU). AKT could induce apoptosis through up-regulation of bax and down-regulation of survivin.
Conclusions: Our data showed that AKT suppressed hepatocellular carcinoma, and the mechanism was associated with regulation of survivin and bax expression, providing support to the clinical use of AKT-based medication to achieve optimized outcome in hepatocellular carcinoma patients.
Methods: AKT was extracted by aqua and organic solutions. The antitumor activity of the organic extract was tested in hepatocellular carcinoma cell lines Huh7 and H22, the latter was also used to establish mouse tumor model. Cell apoptotic rate was analyzed by flow cytometry. In vivo expression of apoptosis associated proteins survivin and bax were analyzed by immunohistochemistry (IHC).
Results: AKT exhibited antitumor activity against hepatocellular carcinoma cell lines. In vivo suppression of H22 was comparable with 5-fluorouracil (5-FU). AKT could induce apoptosis through up-regulation of bax and down-regulation of survivin.
Conclusions: Our data showed that AKT suppressed hepatocellular carcinoma, and the mechanism was associated with regulation of survivin and bax expression, providing support to the clinical use of AKT-based medication to achieve optimized outcome in hepatocellular carcinoma patients.
