S100A6 (calcyclin) enhances the sensitivity to apoptosis via the upregulation of caspase-3 activity in Hep3B cells

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Title
S100A6 (calcyclin) enhances the sensitivity to apoptosis via the upregulation of caspase-3 activity in Hep3B cells
Author(s)
J H Joo; S Y Yoon; J H Kim; S G Paik; Sung Ran Min; J S Lim; In Seong Choe; In Pyo ChoiJae Wha Kim
Bibliographic Citation
Journal of Cellular Biochemistry, vol. 103, no. 4, pp. 1183-1197
Publication Year
2008
Abstract
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.
Keyword
A23187apoptosiscaspase-3EF-handHep3BS100A6
ISSN
0730-2312
Publisher
Wiley
DOI
http://dx.doi.org/10.1002/jcb.21496
Type
Article
Appears in Collections:
Division of Biomaterials Research > Plant Systems Engineering Research > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Division of Biomaterials Research > Cell Factory Research Center > 1. Journal Articles
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