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Seleno‐podophyllotoxin derivatives induce hepatoma SMMC‐7721 cell apoptosis through Bax pathway
Author(s) -
Miao Ruidong,
Han Yin,
An Lizhe,
Yang Jinbo,
Wang Qin
Publication year - 2008
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 - 10.1016/j.cellbi.2007.08.034
Subject(s) - podophyllotoxin , apoptosis , cytoplasm , cytochrome c , mitochondrion , flow cytometry , cell , membrane potential , microbiology and biotechnology , inner mitochondrial membrane , cell cycle , biology , cytotoxicity , chemistry , biochemistry , stereochemistry , in vitro
Podophyllotoxin is a well known anti‐tumor chemical, but because of its strong side effects much effort has been paid to reduce cytotoxicity by modifying its structure. Here, we evaluate the anti‐tumor activity of a new isolated derivative of podophyllotoxin, 4′‐demethyl‐4‐dehydroxy‐4‐seleno‐phenyl‐β‐peltatin‐epipodophyllotoxin (CPZ) and find that CPZ can suppress the proliferation of human hepatoma SMMC‐7721 cells in a dose‐ and time‐dependent manner. Phase‐contrast microscope observation and flow cytometric analysis through PI stains showed that the reagents have strong inhibition of SMMC‐7721 cell growth, as the cells were blocked in the G2/M period. Cell apoptosis induced by CPZ was further confirmed by staining with M30 Cytodeath antibody. Rh123 label testing revealed that the mitochondrial membrane potential had been decreased by CPZ treatment. Under the stress of CPZ, cytochrome c was secreted into the cytoplasm by mitochondria, and Bax in cytoplasm was translocated into the mitochondrial membrane. These results suggest that CPZ‐induced apoptosis may work through a Bax‐dependent pathway.