Programmed cell death ligand‐1: A dynamic immune checkpoint in cancer therapy

Kalim, Muhammad; Khan, Muhammad Saleem Iqbal; Zhan, Jun

doi:10.1111/cbdd.13677

Cited by 18 publications

(16 citation statements)

References 114 publications

(148 reference statements)

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“…The present results suggested that miR-142 was downregulated in LAd, and the overexpression of miR-142 contributed to chemosensitivity in ddP-resistant LAd cells. Pd-L1 may promote tumor cell proliferation and differentiation by creating an imbalance between immune cells and the cellular environment (28,29). Pd-L1 is also reported to be involved in the regulation of tumor development.…”

Section: Discussionmentioning

confidence: 99%

FGD5‑AS1 promotes cisplatin resistance of human lung adenocarcinoma cell via the miR‑142‑5p/PD‑L1 axis

et al. 2020

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Previous studies have reported that long non-coding (lnc) RNA FGD5-antisense 1 (FGD5-AS1) promotes tumor proliferation, migration and invasion. Therefore, the present study aimed to elucidate the biological role and underlying molecular mechanisms of FGD5-AS1 in cisplatin (DDP) resistance of lung adenocarcinoma (LAD) cells. The results demonstrated that FGD5-AS1 was highly expressed in DDP-resistant LAD tissues and cells. Knockdown of FGD5-AS1 decreased the proliferative, migratory and invasive abilities of DDP-resistant LAD cells. Moreover, it was identified that FGD5-AS1 acted as a molecular sponge for microRNA (miR)-142, and FGD5-AS1 enhanced the resistance of A549/DDP cells to DDP by directly interacting with miR-142. Programmed cell death 1 ligand 1 (PD-L1) was also found to be a key effector of the FGD5-AS1/miR-142 axis to regulate the chemoresistance of DDP-resistant LAD cells. In conclusion, the present study demonstrated that FGD5-AS1 increased DDP resistance of LAD via the miR-142/PD-L1 axis, which may offer a novel treatment strategy for patients with DDP-resistant LAD.

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Section: Discussionmentioning

confidence: 99%

FGD5‑AS1 promotes cisplatin resistance of human lung adenocarcinoma cell via the miR‑142‑5p/PD‑L1 axis

et al. 2020

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“…Studies have found that the interaction between PD-1 and PD-L1 is a key therapeutic target for reactivating the immune response against a variety of cancers. Therefore, blocking the PD-1/PD-L1 interaction with an antibody against the PD-L1 molecule is a new therapeutic opportunity for patients with advanced platinum-resistant ovarian cancer (102)(103)(104). The human immunoglobulin G1 monoclonal antibody avelumab has a wild-type Fc region that blocks PD-L1.…”

Section: Cancer Stem Cells (Cscs) the Current Oncology Hypothesismentioning

confidence: 99%

Molecular mechanisms of platinum‑based chemotherapy resistance in ovarian cancer (Review)

et al. 2022

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Cisplatin is one of the most effective chemotherapy drugs for ovarian cancer, but resistance is common. The initial response to platinum-based chemotherapy is as high as 80%, but in most advanced patients, final relapse and death are caused by acquired drug resistance. The development of resistance to therapy in ovarian cancer is a significant hindrance to therapeutic efficacy. The resistance of ovarian cancer cells to chemotherapeutic mechanisms is rather complex and includes multidrug resistance, DNA damage repair, cell metabolism, oxidative stress, cell cycle regulation, cancer stem cells, immunity, apoptotic pathways, autophagy and abnormal signaling pathways. The present review provided an update of recent developments in our understanding of the mechanisms of ovarian cancer platinum-based chemotherapy resistance, discussed current and emerging approaches for targeting these patients and presented challenges associated with these approaches, with a focus on development and overcoming resistance. Contents1. Introduction 2. Literature review methods 3. Molecular mechanisms of platinum-based chemotherapy resistance in ovarian cancer 4. Conclusions

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“…Immune check point proteins such as PD-1 are targeted for restoration of anti-HBV immune response breaking immune tolerance. Preclinically, the combination of an antibody to the PD-1 ligand (programmed death ligand 1) [129] with DNA vaccination resulted in complete viral clearance in a woodchuck model [130], successfully supporting the therapeutic potential of restored T cell response [131]. Indeed, blockade of PD-1 has been shown to partially restore HBV-specific T cell function [126 •• ].…”

Section: Immune-mediated Degradation Of Cccdnamentioning

confidence: 99%

Targeting Viral cccDNA for Cure of Chronic Hepatitis B

Ligat

Goto

Verrier

2020

Curr Hepatology Rep

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Purpose of Review Chronic hepatitis B (CHB), caused by hepatitis B virus (HBV), is a major cause of advanced liver disease and hepatocellular carcinoma (HCC) worldwide. HBV replication is characterized by the synthesis of covalently closed circular (ccc) DNA which is not targeted by antiviral nucleos(t)ide analogues (NUCs) the key modality of standard of care. While HBV replication is successfully suppressed in treated patients, they remain at risk for developing HCC. While functional cure, characterized by loss of HBsAg, is the first goal of novel antiviral therapies, curative treatments eliminating cccDNA remain the ultimate goal. This review summarizes recent advances in the discovery and development of novel therapeutic strategies and their impact on cccDNA biology. Recent Findings Within the last decade, substantial progress has been made in the understanding of cccDNA biology including the discovery of host dependency factors, epigenetic regulation of cccDNA transcription and immune-mediated degradation. Several approaches targeting cccDNA either in a direct or indirect manner are currently at the stage of discovery, preclinical or early clinical development. Examples include genome-editing approaches, strategies targeting host dependency factors or epigenetic gene regulation, nucleocapsid modulators and immune-mediated degradation. Summary While direct-targeting cccDNA strategies are still largely at the preclinical stage of development, capsid assembly modulators and immune-based approaches have reached the clinical phase. Clinical trials are ongoing to assess their efficacy and safety in patients including their impact on viral cccDNA. Combination therapies provide additional opportunities to overcome current limitations of individual approaches.

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Programmed cell death ligand‐1: A dynamic immune checkpoint in cancer therapy

Cited by 18 publications

References 114 publications

FGD5‑AS1 promotes cisplatin resistance of human lung adenocarcinoma cell via the miR‑142‑5p/PD‑L1 axis

FGD5‑AS1 promotes cisplatin resistance of human lung adenocarcinoma cell via the miR‑142‑5p/PD‑L1 axis

Molecular mechanisms of platinum‑based chemotherapy resistance in ovarian cancer (Review)

Targeting Viral cccDNA for Cure of Chronic Hepatitis B

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