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<p>LIM and senescent cell antigen-like domains protein 2 (LIMS2) is a focal adhesion–associated protein involved in cytoskeletal organization and cell–matrix interactions. However, its expression pattern and biological significance in lung adenocarcinoma (LUAD) have not been fully elucidated. Transcriptomic data from The Cancer Genome Atlas were analyzed to assess LIMS2 expression across cancer types and its prognostic relevance in LUAD. Protein–protein interaction analysis and functional enrichment were performed to explore biological processes potentially associated with LIMS2. Gain-of-function experiments were conducted in A549 and NCI-H358 cells to evaluate the effects of LIMS2 overexpression on cell proliferation and migration. In addition, multiple computational algorithms were applied to investigate the relationship between LIMS2 expression, immune cell infiltration, and immune checkpoint–related genes in LUAD. LIMS2 expression was significantly decreased in LUAD tissues compared with normal lung tissues and was associated with poorer clinical outcomes. Functional assays demonstrated that LIMS2 overexpression markedly inhibited LUAD cell proliferation and migratory capacity. Bioinformatic analyses indicated that LIMS2-related genes were mainly enriched in cytoskeleton-associated processes and signaling pathways such as MAPK and Hippo. Immune-related analyses further revealed that LIMS2 expression was significantly correlated with the infiltration of multiple immune cell populations and the expression of immune checkpoint molecules, including PDCD1, CTLA4, and CD274. These results suggest that LIMS2 is frequently downregulated in LUAD and may be associated with tumor progression through its involvement in cellular behavior and the tumor immune landscape. LIMS2 may serve as a potential prognostic biomarker and warrants further investigation in lung adenocarcinoma.</p>

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LIMS2 downregulation is associated with tumor progression and immune landscape alterations in lung adenocarcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月27日

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  • Huanhuan Wang,
  • Chunyu Li,
  • Yuan Gao,
  • Wanqi Zeng,
  • Xingye Li,
  • Jingjing Wang,
  • Weiwei Wang,
  • Wenting Yang,
  • Yaqiong Dong

摘要

LIM and senescent cell antigen-like domains protein 2 (LIMS2) is a focal adhesion–associated protein involved in cytoskeletal organization and cell–matrix interactions. However, its expression pattern and biological significance in lung adenocarcinoma (LUAD) have not been fully elucidated. Transcriptomic data from The Cancer Genome Atlas were analyzed to assess LIMS2 expression across cancer types and its prognostic relevance in LUAD. Protein–protein interaction analysis and functional enrichment were performed to explore biological processes potentially associated with LIMS2. Gain-of-function experiments were conducted in A549 and NCI-H358 cells to evaluate the effects of LIMS2 overexpression on cell proliferation and migration. In addition, multiple computational algorithms were applied to investigate the relationship between LIMS2 expression, immune cell infiltration, and immune checkpoint–related genes in LUAD. LIMS2 expression was significantly decreased in LUAD tissues compared with normal lung tissues and was associated with poorer clinical outcomes. Functional assays demonstrated that LIMS2 overexpression markedly inhibited LUAD cell proliferation and migratory capacity. Bioinformatic analyses indicated that LIMS2-related genes were mainly enriched in cytoskeleton-associated processes and signaling pathways such as MAPK and Hippo. Immune-related analyses further revealed that LIMS2 expression was significantly correlated with the infiltration of multiple immune cell populations and the expression of immune checkpoint molecules, including PDCD1, CTLA4, and CD274. These results suggest that LIMS2 is frequently downregulated in LUAD and may be associated with tumor progression through its involvement in cellular behavior and the tumor immune landscape. LIMS2 may serve as a potential prognostic biomarker and warrants further investigation in lung adenocarcinoma.