Cited by 681Cancer Immunotherapy and BiomarkersT-cell and B-cell ImmunologyImmunotherapy and Immune Responses

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Regulation of PD-L1 expression in the tumor microenvironment

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Yi, Ming, Niu, Mengke, Xu, Linping, Luo, Suxia, Wu, Kongming·2021·Journal of Hematology & Oncology

DOI 10.1186/s13045-020-01027-5PMC PMC7792099

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Abstract

Programmed death-ligand 1 (PD-L1) on cancer cells engages with programmed cell death-1 (PD-1) on immune cells, contributing to cancer immune escape. For multiple cancer types, the PD-1/PD-L1 axis is the major speed-limiting step of the anti-cancer immune response. In this context, blocking PD-1/PD-L1 could restore T cells from exhausted status and eradicate cancer cells. However, only a subset of PD-L1 positive patients benefits from α-PD-1/PD-L1 therapies. Actually, PD-L1 expression is regulated by various factors, leading to the diverse significances of PD-L1 positivity. Understanding the mechanisms of PD-L1 regulation is helpful to select patients and enhance the treatment effect. In this review, we focused on PD-L1 regulators at the levels of transcription, post-transcription, post-translation. Besides, we discussed the potential applications of these laboratory findings in the clinic.

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Fig. 1 The regulators of PD-L1 expression. PD-L1 abundance is regulated by genomic alterations (amplification or translocation), epigenetic modifications (methylation of histone or CpG island, and histone acetylation), transcriptional regulation (inflammatory stimuli and oncogenic signals), post-transcriptional regulation (miRNA, the status of 3′- UTR, RAS, and Angiotensin II), and post-translational modification (ubiquitination, phosphorylation, glycosylation, palmitoylation). H3K4me3: tri-methylation of histone H3 on lysine 4; H3K27me3: tri-methylation of histone H3 on lysine 27; EGFR: epidermal growth factor receptor; IRF: interferon-responsive factor; IFN: interferon; DSB: double-strand break; GSK3β: glycogen synthase kinase 3β; PI3K: phosphoinositide 3-kinase; NF-κB: Nuclear factor kappa-B; HIF-1α: hypoxia-inducible factor-1α; ALK: Anaplastic lymphoma kinase; ER: endoplasmic reticulumCC BY · PubMed Central

Fig. 2 The current immune checkpoint inhibitor therapy could be further enhanced by regulating PD-L1 expression. Agents regulating PD-L1 expression might have a synergistic effect with the current immune checkpoint inhibitors. For example, targeting therapies such as CDK4/6 inhibitor upregulated PD-L1 expression and promoted immune escape. This treatment-induced immune evasion could be overcome by combination therapies containing α-PD-1/PD-L1 (the left panel). Besides, adjuvant treatment regulating PD-L1 expression might elevate the sensitivity to α-PD-1/PD-L1 or other immune checkpoint inhibitors. For instance, metformin downregulated PD-L1 by promoting endoplasmic-reticulum-associated degradation, and the combination therapy of metformin and α-CTLA-4 had a synergistic antitumor activity (the right panel). CDK: cyclin-dependent kinase; CTLA-4: cytotoxic T Lymphocyte antigen 4; ER: endoplasmic reticulumCC BY · PubMed Central

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(Im)maturity in Tumor Ecosystem
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Authors: Yi, M., Niu, M., Xu, L., Luo, S., & Wu, K.
Affiliations: Tongji Hospital (CN)
Zhengzhou University (CN)
Corresponding author: Luo, Suxia
Wu, Kongming
ORCID: Yi, Ming
Niu, Mengke
Luo, Suxia
Wu, Kongming
Venue: Journal of Hematology & Oncology
Publisher: Springer Science and Business Media LLC
Published: 2021-01-07
Volume: 14
Issue: 1
Pages: 10-10
ISSN: 1756-8722 (ISSN-L)
DOI: 10.1186/s13045-020-01027-5
PMC: PMC7792099
OpenAlex: W3118950316
Cited by: 681
References: 153
Citations by year: 2026: 114 · 2025: 108 · 2024: 169 · 2023: 130 · 2022: 113 · 2021: 47
FWCI: 13.99
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0 (tdm)
creativecommons.org/licenses/by/4.0 (vor)
Locations: Journal of Hematology & Oncology (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, other-oa)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: National Natural Science Foundation of China (81874120, 82073370)
Topics: Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Keywords: PD-L1, PD-1/PD-L1 axis, tumor microenvironment, tumor immune evasion, transcriptional regulation, post-transcriptional regulation, post-translational regulation, T cell exhaustion, immune checkpoint inhibitors, predictive biomarkers
MeSH terms: Animals, Humans, Neoplasms, Protein Processing, Post-Translational, Transcriptional Activation, Gene Expression Regulation, Neoplastic, Tumor Escape, Epigenesis, Genetic, Tumor Microenvironment, B7-H1 Antigen

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