ORIGINAL RESEARCH article
Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1595900
This article is part of the Research TopicImmuno-Metabolic Interactions and Cancer Progression in the Tumor MicroenvironmentView all 3 articles
FGA Modulates Immune Infiltration and Tumor progression via SLC7A11/xCT-Mediated Disulfidptosis in the Tumor Microenvironment of Lung Adenocarcinoma
Provisionally accepted
- 1Department of Hematology, Affiliated Hospital of Jining Medical University, 272000, Jining, China
- 2Weishan County People's Hospital, 272000, Jining, China
- 3Department of Wound Reconstructive Surgery, Tongji Hospital, School of Medicine, Tongji University, 200065, Shanghai, China
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Emerging evidence highlights the tumor microenvironment (TME) crucial role in driving tumorigenesis and malignant progression. Disulfidptosis has recently been discovered as a non-apoptotic cell death mechanism triggered by intracellular disulfide stress. However, the impact of disulfidptosis within the dynamic modulation of the immune and stromal components in TME of lung adenocarcinoma (LUAD) remains poorly characterized. In the presented study, RNA-seq and clinical data of LUAD patients were downloaded from TCGA, screening for genes associated with disulfidptosis and immune infiltration, revealed that fibrinogen alpha chain (FGA) modulates immune infiltration via disulfidptosis regulation.We also in vitro experiments identified FGA suppression abrogates disulfidptosis through SLC7A11/xCT downregulation, attenuated disulfidptosis while concurrently enhancing malignant phenotypes, including cellular proliferation, migratory capacity, and invasive potential in lung adenocarcinoma models, this study reveals that FGA functions as a tumor suppressor that can impede the tumorigenesis of LUAD by inhibiting xCT expression, suggesting a novel therapeutic strategy enabling modulation of disulfidptosis for LUAD management.
Keywords: Immune infiltration, disulfidptosis, Tumor Microenvironment, non-small-cell lung cancer, Lung Adenocarcinoma
Received: 18 Mar 2025; Accepted: 03 Jul 2025.
Copyright: © 2025 Li, Jia, Yang, Guo, Tao and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Gen Li, Department of Wound Reconstructive Surgery, Tongji Hospital, School of Medicine, Tongji University, 200065, Shanghai, China
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