Mechanisms Controlling PD-L1 Expression in Cancer

The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed death-ligand 1 (PD-L1; encoded by the CD274 gene), is a major co-inhibitory checkpoint signaling that controls T cell activities. Various types of ca...

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Published in:	Molecular cell Vol. 76; no. 3; p. 359
Main Authors:	Cha, Jong-Ho, Chan, Li-Chuan, Li, Chia-Wei, Hsu, Jennifer L, Hung, Mien-Chie
Format:	Journal Article
Language:	English
Published:	United States 07.11.2019
Subjects:	Animals Antineoplastic Agents, Immunological - therapeutic use B7-H1 Antigen - antagonists & inhibitors B7-H1 Antigen - genetics B7-H1 Antigen - immunology B7-H1 Antigen - metabolism Biomarkers, Tumor - antagonists & inhibitors Biomarkers, Tumor - genetics Biomarkers, Tumor - immunology Biomarkers, Tumor - metabolism Gene Expression Regulation, Neoplastic Humans Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - genetics Neoplasms - immunology Neoplasms - metabolism Protein Processing, Post-Translational RNA Processing, Post-Transcriptional Signal Transduction Transcription, Genetic Tumor Escape
ISSN:	1097-4164, 1097-4164
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Abstract	The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed death-ligand 1 (PD-L1; encoded by the CD274 gene), is a major co-inhibitory checkpoint signaling that controls T cell activities. Various types of cancers express high levels of PD-L1 and exploit PD-L1/PD-1 signaling to evade T cell immunity. Blocking the PD-L1/PD-1 pathway has consistently shown remarkable anti-tumor effects in patients with advanced cancers and is recognized as the gold standard for developing new immune checkpoint blockade (ICB) and combination therapies. However, the response rates of anti-PD-L1 have been limited in several solid tumors. Therefore, furthering our understanding of the regulatory mechanisms of PD-L1 can bring substantial benefits to patients with cancer by improving the efficacy of current PD-L1/PD-1 blockade or other ICBs. In this review, we provide current knowledge of PD-L1 regulatory mechanisms at the transcriptional, posttranscriptional, post-translational, and extracellular levels, and discuss the implications of these findings in cancer diagnosis and immunotherapy.
AbstractList	The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed death-ligand 1 (PD-L1; encoded by the CD274 gene), is a major co-inhibitory checkpoint signaling that controls T cell activities. Various types of cancers express high levels of PD-L1 and exploit PD-L1/PD-1 signaling to evade T cell immunity. Blocking the PD-L1/PD-1 pathway has consistently shown remarkable anti-tumor effects in patients with advanced cancers and is recognized as the gold standard for developing new immune checkpoint blockade (ICB) and combination therapies. However, the response rates of anti-PD-L1 have been limited in several solid tumors. Therefore, furthering our understanding of the regulatory mechanisms of PD-L1 can bring substantial benefits to patients with cancer by improving the efficacy of current PD-L1/PD-1 blockade or other ICBs. In this review, we provide current knowledge of PD-L1 regulatory mechanisms at the transcriptional, posttranscriptional, post-translational, and extracellular levels, and discuss the implications of these findings in cancer diagnosis and immunotherapy. The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed death-ligand 1 (PD-L1; encoded by the CD274 gene), is a major co-inhibitory checkpoint signaling that controls T cell activities. Various types of cancers express high levels of PD-L1 and exploit PD-L1/PD-1 signaling to evade T cell immunity. Blocking the PD-L1/PD-1 pathway has consistently shown remarkable anti-tumor effects in patients with advanced cancers and is recognized as the gold standard for developing new immune checkpoint blockade (ICB) and combination therapies. However, the response rates of anti-PD-L1 have been limited in several solid tumors. Therefore, furthering our understanding of the regulatory mechanisms of PD-L1 can bring substantial benefits to patients with cancer by improving the efficacy of current PD-L1/PD-1 blockade or other ICBs. In this review, we provide current knowledge of PD-L1 regulatory mechanisms at the transcriptional, posttranscriptional, post-translational, and extracellular levels, and discuss the implications of these findings in cancer diagnosis and immunotherapy.The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed death-ligand 1 (PD-L1; encoded by the CD274 gene), is a major co-inhibitory checkpoint signaling that controls T cell activities. Various types of cancers express high levels of PD-L1 and exploit PD-L1/PD-1 signaling to evade T cell immunity. Blocking the PD-L1/PD-1 pathway has consistently shown remarkable anti-tumor effects in patients with advanced cancers and is recognized as the gold standard for developing new immune checkpoint blockade (ICB) and combination therapies. However, the response rates of anti-PD-L1 have been limited in several solid tumors. Therefore, furthering our understanding of the regulatory mechanisms of PD-L1 can bring substantial benefits to patients with cancer by improving the efficacy of current PD-L1/PD-1 blockade or other ICBs. In this review, we provide current knowledge of PD-L1 regulatory mechanisms at the transcriptional, posttranscriptional, post-translational, and extracellular levels, and discuss the implications of these findings in cancer diagnosis and immunotherapy.
Author	Chan, Li-Chuan Li, Chia-Wei Hsu, Jennifer L Hung, Mien-Chie Cha, Jong-Ho
Author_xml	– sequence: 1 givenname: Jong-Ho surname: Cha fullname: Cha, Jong-Ho organization: Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Biomedical Sciences, College of Medicine, Inha University, Incheon 22212, Korea – sequence: 2 givenname: Li-Chuan surname: Chan fullname: Chan, Li-Chuan organization: Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA – sequence: 3 givenname: Chia-Wei surname: Li fullname: Li, Chia-Wei organization: Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA – sequence: 4 givenname: Jennifer L surname: Hsu fullname: Hsu, Jennifer L organization: Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA – sequence: 5 givenname: Mien-Chie surname: Hung fullname: Hung, Mien-Chie email: mhung@cmu.edu.tw organization: Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate Institute of Biomedical Sciences and Center for Molecular Medicine, and Office of the President, China Medical University, Taichung 404, Taiwan. Electronic address: mhung@cmu.edu.tw
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/31668929$$D View this record in MEDLINE/PubMed
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PublicationTitle	Molecular cell
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PublicationYear	2019
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Snippet	The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed... The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed...
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SubjectTerms	Animals Antineoplastic Agents, Immunological - therapeutic use B7-H1 Antigen - antagonists & inhibitors B7-H1 Antigen - genetics B7-H1 Antigen - immunology B7-H1 Antigen - metabolism Biomarkers, Tumor - antagonists & inhibitors Biomarkers, Tumor - genetics Biomarkers, Tumor - immunology Biomarkers, Tumor - metabolism Gene Expression Regulation, Neoplastic Humans Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - genetics Neoplasms - immunology Neoplasms - metabolism Protein Processing, Post-Translational RNA Processing, Post-Transcriptional Signal Transduction Transcription, Genetic Tumor Escape
Title	Mechanisms Controlling PD-L1 Expression in Cancer
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Volume	76
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