Relationship Between Programmed Death-ligand 1 and Clinicopathological Characteristics in Non-small Cell Lung Cancer Patients

Chen, Yanyan; Liu-bo, Wang; Zhu, Huili; Li, Xiangyang; Zhu, Yanping; Yin, Yun; Lu, Fei; Wang, Zili; Qu, Jieming

doi:10.1016/s1001-9294(13)60040-1

Cited by 37 publications

(23 citation statements)

References 13 publications

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“…PD‐L1 that is expressed in cancer cells could specifically bind to the receptor (PD‐1) on the surface of activated T cells in the tumor microenvironment and transmit negative regulatory signals to inhibit T cell activation, proliferation or cytokine secretion [20,21]. The rates of PD‐L1 expression are quite different (25–65%) in non‐small‐cell lung cancer as determined by immunohistochemistry [22–24]. The difference may be a result of various factors, such as the regional specificity of the tumor, differences in the experimental method or criteria for judgment, or the pathological state of the patient.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐155‐5p suppresses PD‐L1 expression in lung adenocarcinoma

et al. 2020

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MiR‐155‐5p is a key oncogenic microRNA that maintains immune homeostasis and mediates cross‐talk between inflammation and tumorigenesis. High expression of programmed death ligand‐1 (PD‐L1) also plays an important role in immune tolerance in tumors. The present study aimed to explore the relationship between miR‐155‐5p and PD‐L1 in lung adenocarcinoma (LUAD) cells A549 and H1650. The expression levels of miR‐155‐5p and PD‐L1 in LUAD patients were detected by a quantitative reverse transcriptase‐polymerase chain reaction (qRT‐PCR) and mimics of miR‐155‐5p were used to model increased expression in A549 or H1650 cells. After 24 h, we measured levels of PD‐L1 by qRT‐PCR, western blotting and flow cytometry. In addition, we identified two sites in the PD‐L1 3′‐UTR (5′‐AGCAUUA‐3′ and 5′‐GCAUUAA‐3′) that can be bound by miR‐155‐5p using TargetScan (http://www.targetscan.org). Compared to normal tissue, miR‐155‐5p was overexpressed in tumor tissue (P = 0.0456), whereas the expression of PD‐L1 was not significantly different (P = 0.1349). The expression levels of miR‐155‐5p and PD‐L1 were negatively correlated (r = −0.6409, P = 0.0459 and r = −0.7544, P = 0.0117). Exogenous overexpression of miR‐155‐5p decreased the mRNA, total protein and membrane protein expression levels of PD‐L1 both in A549 and H1650 cells (P < 0.05). Taken together, our data suggest that miR‐155‐5p may suppress the expression of PD‐L1 in LUAD.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐155‐5p suppresses PD‐L1 expression in lung adenocarcinoma

et al. 2020

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“…PD-L1 expression has been reported to be associated with vascular invasion and higher-grade differentiation but improved relapse free survival [45]. PD-L1 expression is associated with increased macrophages [47], increased dendritic cells [50] and increased inflammatory infiltrate [46]. In contrast, one study found PD-L1 expression was inversely related to TILs [51].…”

Section: Co-inhibitory Interactionsmentioning

confidence: 99%

Immunotherapy in the treatment of non-small cell lung cancer

et al. 2014

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Advances in the understanding of the role of the immune system in tumor immunosurveillance have resulted in the recognition that tumors can evade immune destruction via the dysregulation of co-inhibitory or checkpoint signals. This has led to the development of a generation immunotherapeutic agents targeting the immune checkpoint pathway. Recent early phase studies of immune checkpoint modulators, such as CTLA-4, PD-1 and PD-L1 inhibitors in NSCLC have reported promising results with prolonged clinical responses and tolerable toxicity. This article provides an overview of co-stimulatory and inhibitory molecules that regulate the immune response to tumors, recent therapies that have been developed to exploit these interactions and the role of predictive biomarkers in treatment selection.

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“…Recently, it is reported that PD-L1 was expressed in 19.6% to 65.3% of NSCLC, 7,[11][12][13][14] and that EGFR mutation status was associated with PD-L1 expression. 15,16 More interestingly, PD-L1 positive patients treated with EGFR-TKIs have higher response rate and longer time to progression (TTP) compared with PD-L1 negative patients.…”

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confidence: 99%

Upregulation of PD-L1 by EGFR Activation Mediates the Immune Escape in EGFR-Driven NSCLC: Implication for Optional Immune Targeted Therapy for NSCLC Patients with EGFR Mutation

Chen

Fang

Zhan

et al. 2015

Journal of Thoracic Oncology

566

542

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Our results imply that EGFR-TKIs could not only directly inhibit tumor cell viability but also indirectly enhance antitumor immunity through the downregulation of PD-L1. Anti-PD-1/PD-L1 antibodies could be an optional therapy for EGFR-TKI sensitive patients, especially for EGFR-TKIs resistant NSCLC patients with EGFR mutation. Combination of EGFR-TKIs and anti-PD-1/PD-L1 antibodies treatment in NSCLC is not supported by the current study but warrant more studies to move into clinical practice.

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Relationship Between Programmed Death-ligand 1 and Clinicopathological Characteristics in Non-small Cell Lung Cancer Patients

Abstract: PD-L1, secreted from TAM, might induce cancer cells apoptosis, and decrease lymph node metastasis.

Cited by 37 publications

References 13 publications

MicroRNA‐155‐5p suppresses PD‐L1 expression in lung adenocarcinoma

MicroRNA‐155‐5p suppresses PD‐L1 expression in lung adenocarcinoma

Immunotherapy in the treatment of non-small cell lung cancer

Upregulation of PD-L1 by EGFR Activation Mediates the Immune Escape in EGFR-Driven NSCLC: Implication for Optional Immune Targeted Therapy for NSCLC Patients with EGFR Mutation

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