ArticleWorld journal of oncology2024
Interferon Gamma Receptor 2 Collaborates With Circular RNA/MicroRNA to Modulate Programmed Cell Death-Ligand 1 Levels in Nasopharyngeal Carcinoma.
Article in World journal of oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Core regulatory mechanisms of the PD-L1 axis and clinical strategies for immune escape and immunotherapy response in nasopharyngeal carcinoma.Translational oncology · 2026Review
- Review
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Authors and funding
8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: The effectiveness of immune checkpoint therapy highlights the need to understand abnormal programmed cell death protein-1 (PD-1) expression in nasopharyngeal carcinoma (NPC), especially when treatments fail, or resistance develops. Interferon gamma (IFN-γ) signaling is crucial for regulating programmed cell death-ligand 1 (PD-L1) expression. Our study focuses on interferon gamma receptor 2 (IFNGR2), an essential part of the IFN-γ pathway, and its impact on malignant traits in NPC. Methods: The expression levels of IFNGR2 and PD-L1 were accessed using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). To understand the cellular phenotypic effects, small interfering RNA (siRNA)/short hairpin RNA (shRNA) knockdown techniques were used to evaluate cell viability, clonogenic survival, migration and invasion, immunohistochemistry, and tumor formation assays. The relationship between IFNGR2 and microRNAs (miRNAs)/circular RNAs (circRNAs) will be verified using methods such as circRNA stability assay, rescue, and dual-luciferase reporter assay. Results: IFNGR2 was significantly overexpressed in NPC, and its expression positively correlated with PD-L1 levels. This overexpression contributed to increased cell proliferation, migration, invasion, clonogenicity, and tumor growth. Additionally, we identified an oncogenic circular RNA, circ_001377, and uncovered a novel mechanism by which upregulation of circ_001377 competitively bound to miR-498-3p. This interaction reduced miR-498-3p's ability to target IFNGR2. As a result, the diminished miR-498-3p led to increased IFNGR2 expression, which subsequently activated the IFN-γ signaling pathway and drove abnormal PD-L1 expression. Conclusions: IFNGR2 is an oncogenic factor in NPC. The circ_001377/miR-498-3p interaction drives IFNGR2 upregulation and PD-L1 overexpression, suggesting that targeting this axis could improve therapeutic outcomes.
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