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S100A6 (calcyclin) enhances the sensitivity to apoptosis via the upregulation of caspase‐3 activity in Hep3B cells
Author(s) -
Joo Joung Hyuck,
Yoon Sun Young,
Kim Joo Heon,
Paik SangGi,
Min Sung Ran,
Lim JongSeok,
Choe In Seong,
Choi Inpyo,
Kim Jae Wha
Publication year - 2007
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21496
Subject(s) - downregulation and upregulation , apoptosis , gene knockdown , microbiology and biotechnology , programmed cell death , transfection , caspase , caspase 3 , caspase 2 , intracellular , biology , mutant , cell , cell culture , chemistry , biochemistry , genetics , gene
S100A6 (calcyclin) is a small calcium‐binding protein which has been implicated in several cellular processes such as cell cycle progression, cytoskeleton rearrangement, and exocytosis. Also the upregulation of S100A6 has been reported in a variety of tumors and linked to metastasis. However, exact intracellular roles of S100A6 related with apoptosis have not been clarified yet. Here we demonstrated that the upregulation of S100A6 enhances the cell death rate compared to the control under the apoptotic conditions. In exogenously S100A6 induced Hep3B cells, cell viability was significantly decreased compared with mock and S100A6‐knockdown cells under calcium ionophore A23187 treatment. The exogenously introduced S100A6 significantly affected the caspase‐3‐like activity in programmed cell death through the enhanced caspase‐3 expression, which was verified by promoter assay in wild or mutant S100A6‐transfected Hep3B cells. Next, the promoter activity of caspase‐3 was increased by 2.5‐folds in wild‐type S100A6‐transfected cells compared to mutant 2 (E67K, mutant of EF‐hand motif) or control. Our results suggest that S100A6 might be involved in the processing of apoptosis by modulating the transcriptional regulation of caspase‐3. J. Cell. Biochem. 103: 1183–1197, 2008. © 2007 Wiley‐Liss, Inc.