regulation of pd-l1: emerging routes for targeting tumor immune evasion

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ID: 248270
2018
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Abstract
Immune checkpoint blockade therapies (ICBTs) targeting programmed cell death 1 (PD-1) and its ligand programmed death ligand-1 (PD-L1/B7-H1/CD274) have exhibited momentous clinical benefits and durable responses in multiple tumor types. However, primary resistance is found in considerable number of cancer patients, and most responders eventually develop acquired resistance to ICBT. To tackle these challenges, it is essential to understand how PD-L1 is controlled by cancer cells to evade immune surveillance. Recent research has shed new light into the mechanisms of PD-L1 regulation at genetic, epigenetic, transcriptional, translational, and posttranslational levels. In this work, we systematically discuss the mechanisms that control the gene amplification, epigenetic alteration, transcription, subcellular transportation and posttranscriptional modification of PD-L1 in cancer cells. We further categorize posttranscriptional PD-L1 regulations by the molecular modification of PD-L1, including glycosylation, phosphorylation, ubiquitination, deubiquitination, and lysosomal degradation. These findings may provide new routes for targeting tumor immune escape and catalyze the development of small molecular inhibitors of PD-L1 in addition to existing antibody drugs.
Reference Key
wang2018frontiersregulation Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Yiting Wang;Huanbin Wang;Han Yao;Chushu Li;Jing-Yuan Fang;Jie Xu
Journal chemical research in chinese universities
Year 2018
DOI
10.3389/fphar.2018.00536
URL
https://www.frontiersin.org/article/10.3389/fphar.2018.00536/full
Keywords
gene expression immunotherapy pd-l1 post-translational modification pharmacology

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