계명대학교 의학도서관 Repository

Over-expression of Reticulon 3 (RTN3) enhances TRAIL-mediated apoptosis via up-regulation of death receptor 5 (DR5) and down-regulation of c-FLIP

Metadata Downloads
Author(s)
권택규
Alternative Author(s)
Kwon, Taeg Kyu
Publication Year
2009
Abstract
Reticulons (RTNs) are a group of integral membrane proteins that have no homology to other known apoptosis-related domains. Herein, we found that RTN3 overexpressing Caki cells were sensitive to TRAIL-mediated apoptosis. RTN3-induced down-regulation of c-FLIP was recovered by pan-caspase inhibitor, z-VAD to basal levels in TRAIL-treated cells. The forced expression of c-FLIP attenuated the TRAIL-mediated apoptosis in RTN3 over-expressing cells. In addition, RTN3 over-expression provoked the enhanced protein levels in DR4 and DR5 as well as levels in DR5 surface protein but slight increase in DR4 surface protein. RTN3-mediated enhancement of TRAIL-induced apoptosis was markedly blocked by the DR5/Fc chimera or DR5 siRNA, indicating that the sensitization by RTN3 was mainly mediated through interactions of TRAIL with its receptors, DR5. Over-expression of RTN3 also enhanced TNF-α and Fas-mediated apoptosis. Taken together, over-expression of RTN3 might increase DR5 surface protein and concomitantly more activate caspase pathways, which cause the c-FLIP cleavage and enhancement of TRAIL-mediated apoptosis.

Keywords : RTN3; TRAIL; Apoptosis; DR5; c-FLIP
Department
Dept. of Immunology (면역학)
Institute for Medical Science (의과학연구소)
Publisher
School of Medicine
Citation
Cancer Letters, Vol.279(2) : 185-192, 2009
Type
Article
ISSN
0304-3835
DOI
10.1016/j.canlet.2009.01.035
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35323
Authorize & License
  • AuthorizeOpen
  • EmbargoForever
Files in This Item:

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.