Apoptosis-inducing effect of clostridium difficile toxin A on K562 cells and its mechanism.
- Author:
Pei LI
1
;
Che CHEN
;
Ya-Ming XI
;
Hao ZHANG
;
Ming LI
;
Wei DENG
Author Information
1. Institute of Hematology, Department of Hematology, Lanzhou University First Clinical Hospital, Lanzhou 730000, Gansu Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Bacterial Toxins;
pharmacology;
Caspase 3;
metabolism;
Enterotoxins;
pharmacology;
Gene Expression Regulation, Leukemic;
Humans;
K562 Cells;
drug effects;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
bcl-2-Associated X Protein;
metabolism
- From:
Journal of Experimental Hematology
2011;19(3):638-642
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to investigate the growth inhibition and apoptosis-inducing effect of Clostridium difficile toxin A (TcdA) on the leukemia cell line K562. The proliferative activity of K562 cells exposed to Tcd A was tested by MTT assay, cell apoptosis was detected by flow cytometry; immunocytochemistry and colorimetric assay were employed to detect the protein expressions of BCL-2/BAX and the activity of Caspase-3, respectively. The results indicated that the proliferation of K562 cells was inhibited in a time-and dose-dependent manner after exposure to Tcd A for 24, 48 and 72 hours, the cells displayed the typical apoptotic, morphological changes, the expression of BCL-2 protein was down-regulated but the expression of BAX protein was signficantly increased, compared with control group (p < 0.05). In addition, caspase-3 was activated in a concentration-dependent manner. It is concluded that Tcd A inhibits cell growth of K562 by inducing apoptosis, and the up-regulation of BAX protein and activation of caspase-3 may play important roles in these processes.
