Gambogenic Acid Inhibits Basal Autophagy of Drug-Resistant Hepatoma Cells and Improves Its Sensitivity to Adriamycin

  • Wang Meng
    Key Laboratory of Xin’an Medicine, Ministry of Education, Anhui Province Key Laboratory of R&D of Traditional Chinese Medicine, Anhui University of Chinese Medicine
  • Zhan Fan
    Huaibei Maternity & Child Healthcare Hospital
  • Cheng Hui
    Key Laboratory of Xin’an Medicine, Ministry of Education, Anhui Province Key Laboratory of R&D of Traditional Chinese Medicine, Anhui University of Chinese Medicine
  • Li Qinglin
    Key Laboratory of Xin’an Medicine, Ministry of Education, Anhui Province Key Laboratory of R&D of Traditional Chinese Medicine, Anhui University of Chinese Medicine

この論文をさがす

抄録

<p>Gambogenic acid (GNA) is extracted from plant Gamboge, has a wide range of anti-tumor effects. In this paper, we study the inhibitory effect of GNA on the BEL-7402/ADM of hepatoma resistant cell lines and further study the mechanism of action. Cell viability test represented that GNA could improve the sensitivity of hepatoma drug-resistant cell line BEL-7402/ADM to Adriamycin (ADM), and further study by 4′,6-diamidino-2-phenylindole (DAPI) staining and flow cytometry found that GNA could improve the effect of ADM on promoting apoptosis in BEL-7402/ADM cells, and the activation of apoptosis-related protein was significantly increased, and the ratio of Bax to Bcl-2 was significantly increased. Monodansylcadaverine staining and transmission electron microscopy showed that the basal autophagy level of BEL-7402/ADM cells was higher than that of BEL-7402 cells. Further detection of protein expression found that the intracellular LC3-II to LC3-I ratio and Beclin 1 protein expression increased in the combination of GNA and ADM, but the protein level of p62 increased significantly. GNA inhibit protective autophagy in BEL-7402/ADM cells and promote the role of ADM in inducing apoptosis, thereby increasing ADM sensitivity to BEL-7402/ADM cells, and the effect of GNA inhibition of autophagy may be achieved by inhibiting the degradation of autophagosomes.</p>

収録刊行物

被引用文献 (1)*注記

もっと見る

参考文献 (36)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ