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Corticotropin-releasing factor induces immune escape of cervical cancer cells by downregulation of NKG2D

Authors
Song, HyunkeunPark, HyunjinPark, GabinKim, Yeong SeokLee, Hyun-KyungJin, Dong-HoonKang, Hyung-SikCho, Dae-HoHur, Daeyoung
Issue Date
Jul-2014
Publisher
SPANDIDOS PUBL LTD
Keywords
corticotropin-releasing factor; NKG2D ligand; immune escape; natural killer cells
Citation
ONCOLOGY REPORTS, v.32, no.1, pp 425 - 430
Pages
6
Journal Title
ONCOLOGY REPORTS
Volume
32
Number
1
Start Page
425
End Page
430
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10857
DOI
10.3892/or.2014.3191
ISSN
1021-335X
1791-2431
Abstract
Corticotropin-releasing factor (CRF), a coordinator of the body's responses to stress, is found in various cancer tissues and cell lines. However, the exact abilities of CRF to manipulate natural killer (NK) cells during immune response have not been studied. NKG2D is an activating receptor that is expressed on most NK and CD8(+) T cells. MHC class I-related chain A (MICA) and UL16-binding protein (ULBP) 1,2 and 3 are well-known ligands for NKG2D. In the present study, we reported our findings regarding the role of CRF in cervical cancer cell survival. Human cervical cancer cell line, HeLa cells, had significantly higher intracellular expression of UL16-binding protein 2 (ULBP2) following CRF treatment but had only slightly increased surface expression of ULBP2. Notably, MMPi (pan-metalloproteases inhibitor) blocked the release of ULBP2 molecules from the surface of HeLa cells. Furthermore, incubating NK cells with culture supernatants from CRF-treated HeLa cells, which contained soluble NKG2D ligand, reduced NK cell activity by decreasing surface expression of NKG2D. Collectively, downregulation of NKG2D by CRF-induced soluble NKG2D ligand provides a potential mechanism by which cervical cancer cells escape NKG2D-mediated attack under stress conditions.
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