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Background <p>Stomach adenocarcinoma (STAD) is an aggressive malignant tumor. Herein, we characterized the prognosis based on inflammatory response-related features and evaluated their potential impact on survival and immune status of STAD patients.</p> Methods <p>Inflammation-related genes obtained from public databases were used to analyze the inflammatory response scores of STAD samples. The differentially expressed genes (DEGs) between STAD and adjacent gastric tissue were then analyzed using the “limma” package. Genes associated with STAD prognosis were obtained from the intersection of inflammation-related genes and DEGs. The key genes screened by last absolute shrinkage and selection operator (LASSO) Cox and stepwise regression analyses were used to construct prognostic models and nomograms. The tumor immune dysfunction exclusion (TIDE) algorithm was used to assess potential differences in immunotherapy response between high- and low-risk groups and to explore gene mutation signatures using the R software maftools package. In addition, GSEA was used to predict pathway characteristics between different subgroups. Finally, scratch and transwell assays were performed to explore the role of <i>SERPINE1</i> in STAD cells.</p> Results <p>We found that a high-inflammatory group was associated with poor prognosis in STAD patients. 14&#xa0;inflammation-related DEGs out of 126 DEGs were identified to be associated with the prognosis of STAD patients, and the prognostic models and nomograms constructed from the subsequently identified key genes <i>(SLC7A1</i>, <i>CD82</i>, <i>SERPINE1 ROS1</i> and <i>SLC7A2</i>) demonstrated a good predictive performance in terms of prognosis of STAD. Patients in the STAD high-risk group had higher StromalScore and TIDE scores. It was also found that patients in the STAD low-risk group may have a higher mutation burden. Enrichment analysis revealed significant enrichment of epithelial–mesenchymal transition, angiogenesis and KRAS pathways in the high-risk group. In-vitro experiments showed that down-regulation of <i>SERPINE1</i> attenuated the migratory and invasive abilities of AGS cells.</p> Conclusion <p>This study provides new insights into prognostic prediction and immunotherapy for STAD from the perspective of the inflammatory response.</p>

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Predicting immune status and gene mutations in stomach adenocarcinoma patients based on inflammatory response-related prognostic features

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月9日

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  • Huanjun Li,
  • Jingtang Chen,
  • Zhiliang Chen,
  • Jingsheng Liao

摘要

Background

Stomach adenocarcinoma (STAD) is an aggressive malignant tumor. Herein, we characterized the prognosis based on inflammatory response-related features and evaluated their potential impact on survival and immune status of STAD patients.

Methods

Inflammation-related genes obtained from public databases were used to analyze the inflammatory response scores of STAD samples. The differentially expressed genes (DEGs) between STAD and adjacent gastric tissue were then analyzed using the “limma” package. Genes associated with STAD prognosis were obtained from the intersection of inflammation-related genes and DEGs. The key genes screened by last absolute shrinkage and selection operator (LASSO) Cox and stepwise regression analyses were used to construct prognostic models and nomograms. The tumor immune dysfunction exclusion (TIDE) algorithm was used to assess potential differences in immunotherapy response between high- and low-risk groups and to explore gene mutation signatures using the R software maftools package. In addition, GSEA was used to predict pathway characteristics between different subgroups. Finally, scratch and transwell assays were performed to explore the role of SERPINE1 in STAD cells.

Results

We found that a high-inflammatory group was associated with poor prognosis in STAD patients. 14 inflammation-related DEGs out of 126 DEGs were identified to be associated with the prognosis of STAD patients, and the prognostic models and nomograms constructed from the subsequently identified key genes (SLC7A1, CD82, SERPINE1 ROS1 and SLC7A2) demonstrated a good predictive performance in terms of prognosis of STAD. Patients in the STAD high-risk group had higher StromalScore and TIDE scores. It was also found that patients in the STAD low-risk group may have a higher mutation burden. Enrichment analysis revealed significant enrichment of epithelial–mesenchymal transition, angiogenesis and KRAS pathways in the high-risk group. In-vitro experiments showed that down-regulation of SERPINE1 attenuated the migratory and invasive abilities of AGS cells.

Conclusion

This study provides new insights into prognostic prediction and immunotherapy for STAD from the perspective of the inflammatory response.