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RISS 인기검색어
- 검색키워드
- 저자 : Hirohito Yamaguchi (검색결과 2 건)
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Regulation and Role of EZH2 in Cancer
Hirohito Yamaguchi,Mien-Chie Hung 대한암학회 2014 Cancer Research and Treatment Vol.46 No.3
Polycomb repressive complex 2 (PRC2) is the epigenetic regulator that induces histone H3lysine 27 methylation (H3K27me3) and silences specific gene transcription. Enhancer ofzeste homolog 2 (EZH2) is an enzymatic subunit of PRC2, and evidence shows that EZH2plays an essential role in cancer initiation, development, progression, metastasis, and drugresistance. EZH2 expression is indeed regulated by various oncogenic transcription factors,tumor suppressor miRNAs, and cancer-associated non-coding RNA. EZH2 activity is alsocontrolled by post-translational modifications, which are deregulated in cancer. The canonicalrole of EZH2 is gene silencing through H3K27me3, but accumulating evidence showsthat EZH2 methlyates substrates other than histone and has methylase-independentfunctions. These non-canonical functions of EZH2 are shown to play a role in cancerprogression. In this review, we summarize current information on the regulation and rolesof EZH2 in cancer. We also discuss various therapeutic approaches to targeting EZH2.
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Deubiquitination and Stabilization of PD-L1 by CSN5
Lim, Seung-Oe,Li, Chia-Wei,Xia, Weiya,Cha, Jong-Ho,Chan, Li-Chuan,Wu, Yun,Chang, Shih-Shin,Lin, Wan-Chi,Hsu, Jung-Mao,Hsu, Yi-Hsin,Kim, Taewan,Chang, Wei-Chao,Hsu, Jennifer L.,Yamaguchi, Hirohito,Ding Elsevier 2016 Cancer cell Vol.30 No.6
<P><B>Summary</B></P> <P>Pro-inflammatory cytokines produced in the tumor microenvironment lead to eradication of anti-tumor immunity and enhanced tumor cell survival. In the current study, we identified tumor necrosis factor alpha (TNF-α) as a major factor triggering cancer cell immunosuppression against T cell surveillance via stabilization of programmed cell death-ligand 1 (PD-L1). We demonstrated that COP9 signalosome 5 (CSN5), induced by NF-κB p65, is required for TNF-α-mediated PD-L1 stabilization in cancer cells. CSN5 inhibits the ubiquitination and degradation of PD-L1. Inhibition of CSN5 by curcumin diminished cancer cell PD-L1 expression and sensitized cancer cells to anti-CTLA4 therapy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> TNF-α stabilizes cancer cell PD-L1 in response to chronic inflammation </LI> <LI> Activation of NF-κB by TNF-α induces CSN5 expression leading to PD-L1 stabilization </LI> <LI> CSN5 enzyme activity controls T cell suppression via PD-L1 deubiquitination </LI> <LI> Destabilization of PD-L1 by CSN5 inhibitor curcumin benefits anti-CTLA4 therapy </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
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