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<p>​Integrated stress response (ISR) genes are implicated in lung adenocarcinoma (LUAD) prognosis, but their clinical utility remains unexplored. This study aims to identify ISR-related prognostic genes and construct a risk model for LUAD survival prediction.​ LUAD transcriptomic and clinical data were retrieved from public databases. ISR-related genes (ISR-RGs) were screened via differential expression and regression analysis. A risk model and a nomogram integrating clinical indicators were built and validated. Functional enrichment, immune cell infiltration, and RT-qPCR in clinical samples were performed.​​​ Five prognostic genes (<i>AGER</i>, <i>GPX3</i>, <i>CCNA2</i>, <i>KCNK3</i>, and <i>CHEK1</i>) were identified. High-risk patients exhibited poorer survival. The nomogram was able to forecast the survival of LUAD well. Genes were functionally linked to cell cycle and DNA replication and correlated with immune cells (e.g., <i>CCNA2</i> positively with CD4⁺ T cells [cor = 0.52]; <i>CHEK1</i> negatively with memory B cells [cor = − 0.40]). RT-qPCR confirmed dysregulation: <i>AGER</i>,<i> GPX3</i>, and <i>KCNK3</i> downregulated and <i>CHEK1</i> and <i>CCNA2</i> upregulated versus controls. The five prognostic genes pertinent to both LUAD and ISR were identified, and a risk model was constructed for the good prediction of LUAD survival, which offered a fresh outlook for alleviating the poor prognosis of LUAD.</p>

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Identification and validation of prognostic genes associated with integrative stress response in lung adenocarcinoma and construction of the risk models

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月27日

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  • Jianjun Fu,
  • Yunming Tao,
  • Wu Liu

摘要

​Integrated stress response (ISR) genes are implicated in lung adenocarcinoma (LUAD) prognosis, but their clinical utility remains unexplored. This study aims to identify ISR-related prognostic genes and construct a risk model for LUAD survival prediction.​ LUAD transcriptomic and clinical data were retrieved from public databases. ISR-related genes (ISR-RGs) were screened via differential expression and regression analysis. A risk model and a nomogram integrating clinical indicators were built and validated. Functional enrichment, immune cell infiltration, and RT-qPCR in clinical samples were performed.​​​ Five prognostic genes (AGER, GPX3, CCNA2, KCNK3, and CHEK1) were identified. High-risk patients exhibited poorer survival. The nomogram was able to forecast the survival of LUAD well. Genes were functionally linked to cell cycle and DNA replication and correlated with immune cells (e.g., CCNA2 positively with CD4⁺ T cells [cor = 0.52]; CHEK1 negatively with memory B cells [cor = − 0.40]). RT-qPCR confirmed dysregulation: AGER, GPX3, and KCNK3 downregulated and CHEK1 and CCNA2 upregulated versus controls. The five prognostic genes pertinent to both LUAD and ISR were identified, and a risk model was constructed for the good prediction of LUAD survival, which offered a fresh outlook for alleviating the poor prognosis of LUAD.