상세 정보

underline
Metadata Downloads : dc(xml) or Excel
Cited 0 time in scopus ci

Title 

Oligomycin A enhances apoptotic effect of TRAIL through CHOP-mediated death receptor 5 expression

Authors 

L HeJae-Hyuk JangH G ChoiS M LeeM H NanSook-Jung JeongZ DongY T KwonK S LeeK W LeeJ K ChungJong Seog AhnBo Yeon Kim

Publisher 

Wiley-Blackwell

Issue Date 

2013

Citation 

Molecular Carcinogenesis, vol. 52, no. 2, pp. 85-93

Keywords 

ChemosensitizationCHOPDR5Oligomycin ATRAIL

Abstract 

Development of resistance to TNF-related apoptosis-inducing ligand (TRAIL) in tumor cells is one of the important problems in cancer treatment. Despite the previous report demonstrating that oligomycin suppressed TNF-induced apoptosis, in our screening of small molecules enhancing cancer cell death to TRAIL, oligomycin A (OMA) was found to enhance TRAIL-induced apoptosis in HeLa cells. CCAAT/enhancer-binding protein homologous protein (CHOP) was found to directly bind to death receptor 5 (DR5) promoter through endoplasmic reticulum stress (ER-stress) signaling and sensitize the cells to TRAIL. Among ER-stress associated proteins, OMA triggered the inositol-requiring enzyme 1 (IRE1) signaling pathway, leading to X-binding protein 1 (XBP1) splicing, CHOP expression and DR5 upregulation. In contrast, small-interfering RNA (siRNA) of CHOP reduced the number of apoptotic cells in response to the co-treatment of TRAIL and OMA. Collectively, our data suggest that OMA enhances apoptotic death of cervical cancer cells to TRAIL through upregulation of CHOP-mediated DR5 expression following ER-stress.

ISSN 

0899-1987

Link 

http://dx.doi.org/10.1002/mc.21831

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


There are no files associated with this item.
qrcode

FusionCharts.
DSpace Software Coptright(c) 2010 MIT and Hewleft-Packard  /  KRIBB-REPOSITORY ( Email:jakim@kribb.re.kr)