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The Role of Oncogenes and Redox Signaling in the Regulation of PD-L1 in Cancer
Christophe Glorieux1, Xiaojun Xia1, Peng Huang1
1State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Abstract:
Tumor cells can evade the immune system via multiple mechanisms, including the dysregulation of the immune checkpoint signaling. These signaling molecules are important factors that can either stimulate or inhibit tumor immune response. Under normal physiological conditions, the interaction between programmed cell death ligand 1 (PD-L1) and its receptor, programmed cell death 1 (PD-1), negatively regulates T cell function. In cancer cells, high expression of PD-L1 plays a key role in cancer evasion of the immune surveillance and seems to be correlated with clinical response to immunotherapy. As such, it is important to understand various mechanisms by which PD-L1 is regulated. In this review article, we provide an up-to-date review of the different mechanisms that regulate PD-L1 expression in cancer. We will focus on the roles of oncogenic signals (c-Myc, EML4-ALK, K-ras and p53 mutants), growth factor receptors (EGFR and FGFR), and redox signaling in the regulation of PD-L1 expression and discuss their clinical relevance and therapeutic implications. These oncogenic signalings have common and distinct regulatory mechanisms and can also cooperatively control tumor PD-L1 expression. Finally, strategies to target PD-L1 expression in tumor microenvironment including combination therapies will be also discussed.
Insights
Tumor cells evade immune surveillance by upregulating programmed cell death ligand 1 (PD-L1). This review details how oncogenic signals, growth factor receptors, and redox signaling control PD-L1 expression, impacting cancer immunotherapy response.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Tumor cells exploit immune checkpoints, like PD-L1/PD-1 signaling, to evade immune surveillance.
- High PD-L1 expression in cancer is linked to immune evasion and therapeutic response.
- Understanding PD-L1 regulation is crucial for effective cancer immunotherapy.
Purpose of the Study:
- To review mechanisms regulating PD-L1 expression in cancer.
- To explore the roles of oncogenic signals, growth factor receptors, and redox signaling in PD-L1 regulation.
- To discuss the clinical relevance and therapeutic strategies targeting PD-L1.
Main Methods:
- Literature review of mechanisms controlling PD-L1 expression.
- Focus on oncogenic signals (c-Myc, EML4-ALK, K-ras, p53 mutants).
- Analysis of growth factor receptors (EGFR, FGFR) and redox signaling pathways.
Main Results:
- Oncogenic signals, growth factor receptors, and redox signaling are key regulators of PD-L1.
- These pathways exhibit distinct and cooperative mechanisms to control PD-L1 expression.
- PD-L1 regulation impacts tumor immune evasion and response to immunotherapy.
Conclusions:
- Targeting PD-L1 regulatory mechanisms offers therapeutic potential.
- Combination therapies may enhance treatment efficacy by modulating PD-L1.
- Further research into PD-L1 regulation is vital for advancing cancer immunotherapy.
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