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Expression of calbindin-D28k is inversely correlated with proapototic gene expression in hydrogen peroxide-induced cell death in endometrial cancer cells
Author(s) -
EuiMan Jung,
KyungChul Choi,
EuiBae Jeung
Publication year - 2011
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2011.916
Subject(s) - apoptosis , gene knockdown , biology , programmed cell death , cancer research , cancer cell , microbiology and biotechnology , cancer , genetics
Calbindin-D28k (CaBP-28k) is a calcium binding protein important for intracellular Ca2+ buffering and known to have anti-apoptotic properties in neurons, osteoblasts and male germ cells. Although endometrial cancer is a common invasive gynecologic malignancy, the involvement of uterine CaBP-28k in apoptotic signaling of endometrial cancer is poorly understood. The present study investigates the role of CaBP-28k in hydrogen peroxide (H2O2)-induced apoptotic signaling in human endometrial Ishikawa cells. The dose- and time-dependent effect of H2O2 on Bax, p53 and Bcl-2 expression was assessed by Western blot analysis. Treatment of cells with 1 mM H2O2 for 1 h induced an increase in Bax and p53 expression, but the expression of Bcl-2 was not affected by H2O2 treatment. Interestingly, overexpression of CaBP-28k inhibited cell death and caused a decrease in Bax, p53 and caspase 3 expression during H2O2-induced apoptosis, suggesting that CaBP-28k blocks the up-regulation of apoptosis-related gene expression. siRNA knockdown of CaBP-28k resulted in an elevation of H2O2-induced cell death and an increase in Bax, p53 and caspase 3, providing additional evidence that induction of the CaBP-28k gene might be associated with survival signaling during H2O2-mediated cell death. Overall, these results suggest that CaBP-28k expression is inversely correlated with pro-apoptotic gene expression in human endometrial Ishikawa cells.

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