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GTPase IMAP family member 8 (GIMAP8) plays a key role in pathophysiology of several malignancies. The objective of this current research endeavor was to investigate the prognosis value of GIMAP8 in lung adenocarcinoma and examine how it relates to immunity. Expression profiles associated with GIMAP8 and related clinical details were acquired from The Cancer Genome Atlas database, and we conducted survival analysis, enrichment analysis and immune infiltration studies. Additionally, we evaluated the effect of GIMAP8 on radiation resistance of tumor by in vivo and in vitro experiments. Our results showed that lung adenocarcinoma tumor tissues exhibited lower GIMAP8 levels compared to nearby normal tissues. Furthermore, decreased GIMAP8 expression strongly correlated with poorer OS. The expression of GIMAP8 is closely related to the formation of radiation resistance in tumor cells. GSEA identified multiple signaling pathways linked to GIMAP8, including immune-related, chemokine, cell adhesion molecule, and NF-κB signaling pathways. GIMAP8 expression strongly correlated with the expression of immune checkpoint molecules, tumor mutational burden, tumor neoantigen burden, immune cells, and tumor immune microenvironment. GIMAP8 was found to have an inhibitory effect on lung adenocarcinoma and was closely related to the immune response. Moreover, GIMAP8 may also influence radiation resistance in tumors.
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http://dx.doi.org/10.1038/s41598-025-99894-w | DOI Listing |
Br J Cancer
September 2025
Department of Genetics, Institut Curie, PSL Research University, Paris, France.
Background: Identifying molecular alterations specific to advanced lung adenocarcinomas could provide insights into tumour progression and dissemination mechanisms.
Method: We analysed tumour samples, either from locoregional lesions or distant metastases, from patients with advanced lung adenocarcinoma from the SAFIR02-Lung trial by targeted sequencing of 45 cancer genes and comparative genomic hybridisation array and compared them to early tumours samples from The Cancer Genome Atlas.
Results: Differences in copy-number alterations frequencies suggest the involvement in tumour progression of LAMB3, TNN/KIAA0040/TNR, KRAS, DAB2, MYC, EPHA3 and VIPR2, and in metastatic dissemination of AREG, ZNF503, PAX8, MMP13, JAM3, and MTURN.
Cancer Sci
September 2025
Section of Oncopathology and Morphological Pathology, Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Low-density lipoprotein receptor-related protein 11 (LRP11) is reported to be overexpressed in various cancers; however, its functional role in lung adenocarcinoma remains poorly understood. This study aimed to elucidate the tumor-promoting function of LRP11 in lung adenocarcinoma. We assessed the expression and function of LRP11 in lung adenocarcinoma cell lines through both silencing and overexpression experiments.
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September 2025
Department of Epidemiology, School of Public Health, and Key Laboratory of Public Health Safety of Ministry of Education, Fudan University, Shanghai, China
Objectives: Although lung cancer in never smokers (LCNSs) accounts for an estimated 25% of all lung cancer cases, the temporal trends in LCNS incidence and its broader epidemiological patterns remain poorly understood. Our study examines the temporal trends in LCNS incidence and analyses key epidemiological characteristics, specifically, the trends in mortality rates, survival rates and changes in age at onset to illuminate the reasons for temporal trends in LCNS incidence.
Design: Retrospective population-based cohort study.
J Thorac Oncol
September 2025
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea; Emeritus Professor, Seoul National University College of Medicine, Seoul, Republic of Korea.
Introduction: Multifocal subsolid nodules (SSNs) are increasingly detected with widespread lung cancer screening and advanced thoracic imaging, representing a spectrum of multifocal lung adenocarcinomas (LUADs). When synchronous SSNs coexist with a surgically confirmed subsolid LUAD, their trajectories remain poorly understood, contributing to uncertainty regarding optimal management strategies. This study aimed to evaluate the clinical course and impact of synchronous SSNs in such patients and to identify features associated with their progression.
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September 2025
Department of Clinical Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Faculty of Medical Laborat
Cytokines link inflammation to tumorigenesis, but the role of post-translational modifications in regulating their function within the extra-tumoral environment remains poorly defined. Here, we identify tumor-derived tumor necrosis factor (TNF) receptor superfamily member 11B (TR11B) as a key driver of lung adenocarcinoma (LUAD) progression and therapeutic resistance. Mechanistically, O-GlcNAc transferase (OGT)-mediated O-GlcNAcylation at serine 151 stabilizes TR11B and facilitates its interaction with the membrane protein EPS15 homology domain-containing protein 1 (EHD1), promoting cyclin dependent kinase 2 (CDK2) phosphorylation and cell cycle progression.
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