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API5 Confers Tumoral Immune Escape through FGF2-Dependent Cell Survival Pathway

Authors
Noh, Kyung HeeKim, Seok-HoKim, Jin HeeSong, Kwon-HoLee, Young-HoKang, Tae HeungHan, Hee DongSood, Anil K.Ng, JoanneKim, KwangheeSonn, Chung HeeKumar, VinayYee, CassianLee, Kyung-MiKim, Tae Woo
Issue Date
1-7월-2014
Publisher
AMER ASSOC CANCER RESEARCH
Citation
CANCER RESEARCH, v.74, no.13, pp.3556 - 3566
Indexed
SCIE
SCOPUS
Journal Title
CANCER RESEARCH
Volume
74
Number
13
Start Page
3556
End Page
3566
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/97988
DOI
10.1158/0008-5472.CAN-13-3225
ISSN
0008-5472
Abstract
Identifying immune escape mechanisms used by tumors may define strategies to sensitize them to immunotherapies to which they are otherwise resistant. In this study, we show that the antiapoptotic gene API5 acts as an immune escape gene in tumors by rendering them resistant to apoptosis triggered by tumor antigen-specific T cells. Its RNAi-mediated silencing in tumor cells expressing high levels of API5 restored antigen-specific immune sensitivity. Conversely, introducing API5 into API5(low) cells conferred immune resistance. Mechanistic investigations revealed that API5 mediated resistance by upregulating FGF2 signaling through a FGFR1/PKC delta/ERK effector pathway that triggered degradation of the proapoptotic molecule BIM. Blockade of FGF2, PKC delta, or ERK phenocopied the effect of API5 silencing in tumor cells expressing high levels of API5 to either murine or human antigen-specific T cells. Our results identify a novel mechanism of immune escape that can be inhibited to potentiate the efficacy of targeted active immunotherapies. (C) 2014 AACR.
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