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Epstein-Barr virus (EBV) infection is an established cause of nasopharyngeal carcinoma (NPC) and is involved in a variety of malignant phenotypes, including tumor immune escape. EBV can encode a variety of circular RNAs (circRNA), however, little is known regarding the biological functions of these circRNAs in NPC. In this study, EBV-encoded was found to be highly expressed in NPC where it upregulated PD-L1 expression and inhibited T-cell function and . promoted transcription of PD-L1 by binding the helicase domain of RIG-I and activating transcription factors IRF3 and NF-κB, resulting in tumor immune escape. These results elucidate the biological function of , explain a novel mechanism of immune escape caused by EBV infection, and provide a new immunotherapy target for treating NPC. SIGNIFICANCE: This work demonstrates that binding to RIG-I is essential for the regulation of PD-L1 and subsequent immune escape in nasopharyngeal carcinoma.
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http://dx.doi.org/10.1158/0008-5472.CAN-20-4321 | DOI Listing |
Front Immunol
September 2025
Precision Pharmacy and Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Gliomas are the most common primary malignant tumors of the central nervous system (CNS), and despite progress in molecular diagnostics and targeted therapies, their prognosis remains poor. In recent years, immunotherapy has emerged as a promising treatment modality in cancer therapy. However, the inevitable immune evasion by tumor cells is a key barrier affecting therapeutic efficacy.
View Article and Find Full Text PDFIntroduction: is a spiral-shaped Gram-negative, enterohepatic bacterium classified as a conditional pathogen (pathogenicity group 2). It is known to cause bacteremia and a variety of other diseases in humans. In particular, has been shown to impair intracellular cholesterol metabolism when interacting with macrophages, leading to foam cell formation.
View Article and Find Full Text PDFDiagn Pathol
September 2025
Department of Gastrointestinal Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Background: Gastric cancer is one of the most common cancers worldwide, with its prognosis influenced by factors such as tumor clinical stage, histological type, and the patient's overall health. Recent studies highlight the critical role of lymphatic endothelial cells (LECs) in the tumor microenvironment. Perturbations in LEC function in gastric cancer, marked by aberrant activation or damage, disrupt lymphatic fluid dynamics and impede immune cell infiltration, thereby modulating tumor progression and patient prognosis.
View Article and Find Full Text PDFEsophagus
September 2025
Department of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-Machi, Aoba-Ku, Sendai, Miyagi, Japan.
Background: The cluster of differentiation 47 (CD47)-signal regulatory protein alpha (SIRPα) axis is a key regulator of innate immune surveillance, facilitating the neoplastic evasion of macrophage-mediated phagocytosis. Although this pathway has been implicated in tumor immune escape in multiple malignancies, its clinical and prognostic significance in esophageal squamous cell carcinoma (ESCC) remain to be fully elucidated.
Methods: We retrospectively analyzed 100 patients who underwent esophagectomy for resectable ESCC.
EMBO J
September 2025
Department of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University; Frontier Science Center for Immunology and Metabolism, Taikang Center for Life and Medical Sciences; Wuhan University, Wuhan, 430071, China.
Inadequate antigen presentation by MHC-I in tumor microenvironment (TME) is a common immune escape mechanism. Here, we show that glycine decarboxylase (GLDC), a key enzyme in glycine metabolism, functions as an inhibitor of MHC-I expression in EGFR-activated tumor cells to induce immune escape by a mechanism independent of its enzymatic activity. Upon EGFR activation, GLDC is phosphorylated by SRC and subsequently translocated to the nucleus in human NSCLC cells.
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