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Apoptosis by aloe‐emodin is mediated through down‐regulation of calpain‐2 and ubiquitin‐protein ligase E3A in human hepatoma Huh‐7 cells
Author(s) -
Jeon Won,
Jeon Young Keul,
Nam Myeong Jin
Publication year - 2012
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100723
Subject(s) - apoptosis , calpain , aloe emodin , ubiquitin ligase , mtt assay , chemistry , emodin , microbiology and biotechnology , blot , cancer cell , ubiquitin , cell growth , biology , biochemistry , cancer , genetics , gene , enzyme
Natural flavonoids are associated with anti‐proliferation of cancer growth. However, the antioxidant and anti‐proliferation effects of AE (aloe‐emodin) have not been well studied. We have investigated how AE affects the proliferation of hepatic hepatocellular carcinoma cells and exerts an anti‐cancer effect. The cytotoxic effect of AE was demonstrated using an MTT [3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2 H ‐tetrazolium bromide] assay and Huh‐7 cells were inhibited by AE treatment in both dose‐ and time‐dependent manners. The IC 50 level of AE was ∼75 μM. AE also has anti‐proliferative effects via induction of DNA damage and apoptosis. 2‐DE (two‐dimensional electrophoresis) revealed that several proteins were related to the anti‐cancer effects of AE. CAPN2 (calpain‐2) and UBE3A (ubiquitin‐protein ligase E3A), which are associated with the apoptosis signalling pathway, were verified by Western blotting. AE exhibited potent anti‐proliferative effects on Huh‐7 cells via down‐regulation of CAPN2 and UBE3A. The findings support the possibility of AE being a chemopreventative agent.

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