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Title 

Proteasome inhibitor-I enhances tunicamycin-induced chemosensitization of prostate cancer cells through regulation of NF-κB and CHOP expression

Authors 

P T HuongD O MoonSun Ok KimK E KimSook-Jung JeongKi Won LeeK S LeeJae Hyuik JangR L EriksonJong Seog AhnBo Yeon Kim

Publisher 

Elsevier

Issue Date 

2011

Citation 

Cellular Signalling, vol. 23, no. 5, pp. 857-865

Keywords 

CHOPER-stressNF-κBProteasome inhibitor-1Tunicamycin

Abstract 

Although endoplasmic reticulum (ER) stress induction by some anticancer drugs can lead to apoptotic death of cancer cells, combination therapy with other chemicals would be much more efficient. It has been reported that proteasome inhibitors could induce cancer cell death through ER-stress. Our study, however, showed a differential mechanism of proteasome inhibitor-I (Pro-I)-induced cell death. Pro-I significantly enhanced apoptotic death of PC3 prostate cancer cells pretreated with tunicamycin (TM) while other signaling inhibitors against p38, mitogen activated kinase (MEK) and phosphatidyl-inositol 3-kinase (PI3K) did not, as evidenced by cell proliferation and cell cycle analyses. NF-κB inhibition by Pro-I, without direct effect on ER-stress, was found to be responsible for the TM-induced chemosensitization of PC3 cells. Moreover, TM-induced/enhancer-binding protein (C/EBP) homologous protein (CHOP) expression was enhanced by Pro-I without change in GRP78 expression. CHOP knockdown by siRNA also showed a significant decrease in Pro-I chemosensitization. All these data suggest that although TM could induce both NF-κB activation and CHOP expression through ER-stress, both NF-κB inhibition and increased CHOP level by Pro-I are required for enhanced chemosensitization of PC3 prostate cancer cells. Thus, our study might contribute to the identification of anticancer targets against prostate cancer cells.

ISSN 

0898-6568

Link 

http://dx.doi.org/10.1016/j.cellsig.2011.01.010

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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