دورية أكاديمية
أعرض في EDS

Inhibition of CMTM4 Sensitizes Cholangiocarcinoma and Hepatocellular Carcinoma to T Cell-Mediated Antitumor Immunity Through PD-L1.

التفاصيل البيبلوغرافية
العنوان: Inhibition of CMTM4 Sensitizes Cholangiocarcinoma and Hepatocellular Carcinoma to T Cell-Mediated Antitumor Immunity Through PD-L1.
المؤلفون: Chui NN; Department of Pathology, The University of Hong Kong, Hong Kong., Cheu JW; Department of Pathology, The University of Hong Kong, Hong Kong., Yuen VW; Department of Pathology, The University of Hong Kong, Hong Kong., Chiu DK; Department of Pathology, The University of Hong Kong, Hong Kong., Goh CC; Department of Pathology, The University of Hong Kong, Hong Kong., Lee D; Department of Pathology, The University of Hong Kong, Hong Kong., Zhang MS; Department of Pathology, The University of Hong Kong, Hong Kong.; ShenZhen Hospital, The University of Hong Kong, Shenzhen, China., Ng IO; Department of Pathology, The University of Hong Kong, Hong Kong.; State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong., Wong CC; Department of Pathology, The University of Hong Kong, Hong Kong.; ShenZhen Hospital, The University of Hong Kong, Shenzhen, China.; State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong.
المصدر: Hepatology communications [Hepatol Commun] 2022 Jan; Vol. 6 (1), pp. 178-193. Date of Electronic Publication: 2021 Jul 21.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wolters Kluwer Health, Inc Country of Publication: United States NLM ID: 101695860 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2471-254X (Electronic) Linking ISSN: 2471254X NLM ISO Abbreviation: Hepatol Commun Subsets: MEDLINE
أسماء مطبوعة: Publication: 2023- : [Philadelphia] : Wolters Kluwer Health, Inc.
Original Publication: [Hoboken, NJ] : Wiley Periodicals, Inc. on behalf of the American Association for the Study of Liver Diseases, [2017]-
مواضيع طبية MeSH: Carcinoma, Hepatocellular/*immunology , Cholangiocarcinoma/*immunology , Liver Neoplasms/*immunology , MARVEL Domain-Containing Proteins/*genetics , Programmed Cell Death 1 Receptor/*immunology, Animals ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Cells, Cultured ; Cholangiocarcinoma/drug therapy ; Cholangiocarcinoma/metabolism ; Hepatocytes ; Humans ; Immune Checkpoint Inhibitors/therapeutic use ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; MARVEL Domain-Containing Proteins/antagonists & inhibitors ; Mice, Inbred C57BL ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Up-Regulation ; Mice
مستخلص: Liver cancers consist primarily of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC). Immune checkpoint inhibitors have emerged as promising therapeutic agents against liver cancers. Programmed cell death protein 1 (PD-1) is an immunoinhibitory receptor present on T cells that interacts with its ligand programmed death-ligand 1 (PD-L1) found on cancer cells. Blocking PD-1/PD-L1 binding improves T-cell survival, proliferation and cytotoxicity, which enhances their antitumor activity. Better understanding of the molecular mechanisms governing PD-1/PD-L1 response is essential to the development of predictive markers and therapeutic combinations that could improve the efficiency of anti-PD-1/PD-L1 treatment. Chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing 6 (CMTM6) has been recently identified as a major regulator of PD-L1. Another member in the CMTM family, CKLF-like MARVEL transmembrane domain-containing 4 (CMTM4), has been shown to compensate for the effects of CMTM6 when CMTM6 is lost. Interestingly, we found that CMTM4 is the major regulator of PD-L1 in the context of liver cancer. Up-regulated CMTM4 in patients with HCC and ICC is associated with poor patient survival, potentially due to its function in stabilizing PD-L1 expression, hence facilitating escape from T cell-mediated cytotoxicity. We confirmed the role of CMTM4 as a positive regulator of PD-L1 in multiple HCC and ICC cell lines and demonstrated that CMTM4 stabilizes PD-L1 through posttranslational mechanisms. In vivo, suppression of Cmtm4 inhibited HCC growth and increased CD8 + T-cell infiltration in immunocompetent mice. Furthermore, we found that depletion of CMTM4 sensitized HCC tumor to anti-PD-L1 treatment compared with control. This suggests that CMTM4 expression level could be a predictive marker for patient response to anti-PD-L1 treatment, and CMTM4 depletion can potentially be used to enhance the clinical benefits of anti-PD-L1 immunotherapy in patients with liver cancer.
(© 2021 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of the American Association for the Study of Liver Diseases.)
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المشرفين على المادة: 0 (CMTM4 protein, human)
0 (CMTM4 protein, mouse)
0 (Immune Checkpoint Inhibitors)
0 (MARVEL Domain-Containing Proteins)
0 (PDCD1 protein, human)
0 (Pdcd1 protein, mouse)
0 (Programmed Cell Death 1 Receptor)
تواريخ الأحداث: Date Created: 20210924 Date Completed: 20220304 Latest Revision: 20240226
رمز التحديث: 20240226
مُعرف محوري في PubMed: PMC8710793
DOI: 10.1002/hep4.1682
PMID: 34558800
قاعدة البيانات: MEDLINE
الوصف
تدمد:2471-254X
DOI:10.1002/hep4.1682