US EPA

7422484 

Journal Article 

PUMA and survivin are involved in the apoptosis of HepG2 cells induced by microcystin-LR via mitochondria-mediated pathway 

Ma, J; Feng, Y; Liu, Y; Li, X; , 

2016 

Yes 

Chemosphere
ISSN: 0045-6535
EISSN: 1879-1298 

PERGAMON-ELSEVIER SCIENCE LTD 

OXFORD 

157 

241-249 

English 

27235693 

10.1016/j.chemosphere.2016.05.051 

WOS:000378452400030 

https://linkinghub.elsevier.com/retrieve/pii/S0045653516306993
Exit
 

The present study aimed to determine the cytotoxicity of microcystin-LR (MC-LR) on the human hepatocellular carcinoma (HepG2) cells in order to elucidate the mechanism of apoptosis induced by MC-LR. Morphological evaluation results showed that MC-LR induced time- and concentration-dependent apoptosis in HepG2 cells. The biochemical assays revealed that MC-LR-exposure caused overproduction of reactive oxygen species (ROS), cyclooxygenase-2 activity alteration, cytochrome c release, and remarkable activation of caspase-3 and caspase-9 in HepG2 cells, indicating that MC-LR-induced apoptosis is mediated by mitochondrial pathway. Moreover, we also found that p53 and Bax might play an important role in MC-LR-induced apoptosis in HepG2 cells in which PUMA and survivin were involved. However, further studies are necessary to elucidate the possible functions of PUMA and survivin in MC-LR-induced apoptosis in HepG2 cells. 

Apoptosis; HepG2; Microcystin-LR; Mitochondria-mediated pathway; PUMA; Survivin; Mitochondria; Concentration-dependent; Hepatocellular carcinoma; HepG2; Microcystin-LR; Mitochondrial pathways; PUMA; Reactive oxygen species; Survivin; Cell death; caspase 3; caspase 9; cyclooxygenase 2; cytochrome c; microcystin LR; protein Bax; protein p53; PUMA protein; reactive oxygen metabolite; survivin; apoptosis regulatory protein; BBC3 protein, human; BIRC5 protein, human; cytotoxin; inhibitor of apoptosis protein; microcystin; microcystin LR; oncoprotein; apoptosis; cancer; cells and cell components; concentration (composition); cyanobacterium; enzyme; gene; gene expression; hepatitis; mitochondrion; protein; toxin; apoptosis; Article; bioassay; biochemical analysis; cell structure; controlled study; cytotoxicity; enzyme activity; HepG2 cell line; human; human cell; in vitro study; mitochondrion; protein function; protein secretion; protein synthesis; signal transduction; apoptosis; chemically induced; drug effects; genetics; Hep-G2 cell line; hepatitis; liver tumor; metabolism; risk assessment; Apoptosis; Apoptosis Regulatory Proteins; Cytotoxins; Hep G2 Cells; Hepatitis; Humans; Inhibitor of Apoptosis Proteins; Liver Neoplasms; Microcystins; Proto-Oncogene Proteins; Risk Assessment