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Background <p>Individuals with rheumatoid arthritis (RA) are at a significantly increased risk of developing lung cancer (LC), with a 30%-40% higher incidence compared to the general population. Although a link between the two conditions has been established, the molecular mechanisms and genetic factors remain not fully elucidated. This study aims to uncover the potential associations between LC and RA through an integrative approach of transcriptomics and genomics analysis.</p> Methods <p>We collected whole-genome expression data from patients with LC, RA, and healthy controls. Next-generation sequencing (NGS) was applied to analyze genomic variations in blood samples from RA patients, including those with comorbid LC and interstitial lung disease (ILD). Using bioinformatics tools, we identified differentially expressed genes (DEGs) and conducted an integrative analysis of pathways shared and specific to LC and RA.</p> Results <p>The transcriptome analysis identified 1,051 DEGs common to both LC and RA, with distinct regulatory patterns. Among these, 441 genes were commonly upregulated, 345 were downregulated, and 265 exhibited opposite regulation between the two diseases. After integrating significant genomic mutation data, an additional 92 upregulated, 90 downregulated, and 41 oppositely regulated key genes were identified. Functional and enrichment analyses of these key genes revealed shared alterations in immune-related pathways, particularly the upregulation of viral response and immune signaling pathways, and the downregulation of T-cell receptor (TCR) signaling, T cell activation, and non-coding RNA metabolism. Furthermore, lymphocyte and leukocyte migration, as well as the positive regulation of programmed cell death, showed opposite regulation patterns between the two diseases. Laboratory tests also revealed changes in lymphocytes.</p> Conclusion <p>This study delineates potential common mechanisms between LC and RA, suggesting that an enhanced viral response, attenuated TCR signaling, and reduced T cell activation in the peripheral system may represent shared pathological mechanisms, potentially contributing to the increased LC risk in RA patients. Conversely regulated DEGs may serve as novel biomarkers for pulmonary diseases. The changes in immune-related pathways and their potential association with lymphocyte activity provide new perspectives for understanding the relationship between LC and RA.</p>

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Unraveling the nexus between lung cancer and rheumatoid arthritis using integrative transcriptomics and genomics

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月12日

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  • Heng Li,
  • Liping Ding,
  • Nini Li,
  • Xiaoping Hong,
  • Dongzhou Liu

摘要

Background

Individuals with rheumatoid arthritis (RA) are at a significantly increased risk of developing lung cancer (LC), with a 30%-40% higher incidence compared to the general population. Although a link between the two conditions has been established, the molecular mechanisms and genetic factors remain not fully elucidated. This study aims to uncover the potential associations between LC and RA through an integrative approach of transcriptomics and genomics analysis.

Methods

We collected whole-genome expression data from patients with LC, RA, and healthy controls. Next-generation sequencing (NGS) was applied to analyze genomic variations in blood samples from RA patients, including those with comorbid LC and interstitial lung disease (ILD). Using bioinformatics tools, we identified differentially expressed genes (DEGs) and conducted an integrative analysis of pathways shared and specific to LC and RA.

Results

The transcriptome analysis identified 1,051 DEGs common to both LC and RA, with distinct regulatory patterns. Among these, 441 genes were commonly upregulated, 345 were downregulated, and 265 exhibited opposite regulation between the two diseases. After integrating significant genomic mutation data, an additional 92 upregulated, 90 downregulated, and 41 oppositely regulated key genes were identified. Functional and enrichment analyses of these key genes revealed shared alterations in immune-related pathways, particularly the upregulation of viral response and immune signaling pathways, and the downregulation of T-cell receptor (TCR) signaling, T cell activation, and non-coding RNA metabolism. Furthermore, lymphocyte and leukocyte migration, as well as the positive regulation of programmed cell death, showed opposite regulation patterns between the two diseases. Laboratory tests also revealed changes in lymphocytes.

Conclusion

This study delineates potential common mechanisms between LC and RA, suggesting that an enhanced viral response, attenuated TCR signaling, and reduced T cell activation in the peripheral system may represent shared pathological mechanisms, potentially contributing to the increased LC risk in RA patients. Conversely regulated DEGs may serve as novel biomarkers for pulmonary diseases. The changes in immune-related pathways and their potential association with lymphocyte activity provide new perspectives for understanding the relationship between LC and RA.