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<p>The COVID-19 outbreak in December 2019 in Wuhan, China caused by the highly infectious SARS-CoV-2 induces catastrophic effects on multiple organs and may potentially promote cancer cell proliferation and reawakening in the tumor microenvironment. As the consequences of infection are not fully discovered, we are studying the interplay of SARS-COV-2 infection and Lung cancer. The viral-host protein-protein interaction (PPI) identification could help predict the virus’s behavior and its overlap with other pathogenic pathways. The differential expressed genes (DEGs) of SARS-COV-2 and lung cancer were explored and were used for protein network and cluster generation. Further function enrichment and gene ontology analysis were performed for all the clusters and were compared between the SARS-COV-2 and lung cancer. The analysis revealed 23 common genes and important pathways involved in tumor immune evasion, cancer proliferation, and immune signaling mainly; T cell signaling, IL- 2&amp; IL-4 signaling, interferon signaling, and chemokine signaling pathways. From the common genes identified, biomarkers were obtained; FHL1, CENPE, PAK2, CASP4, FGF2, and SHC2 through overall survival analysis and immune cell infiltration analysis. These findings suggest that SARS-CoV-2 can play a significant role in cancer relapse by supporting tumorigenic conditions in the tumor microenvironment and facilitating tumor cell migration.</p>

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Protein network analysis reveals SARS-CoV-2’s potential mechanisms in accelerating lung cancer tumorigenesis using immune signaling pathways

  • 期刊论文

  • 发表日期：

    2025年11月4日

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  • Navya V B,
  • Ravindra Kumar,
  • Anubhav Mishra,
  • Himanshu Fulmali,
  • Sai Sandeep Reddy

摘要

The COVID-19 outbreak in December 2019 in Wuhan, China caused by the highly infectious SARS-CoV-2 induces catastrophic effects on multiple organs and may potentially promote cancer cell proliferation and reawakening in the tumor microenvironment. As the consequences of infection are not fully discovered, we are studying the interplay of SARS-COV-2 infection and Lung cancer. The viral-host protein-protein interaction (PPI) identification could help predict the virus’s behavior and its overlap with other pathogenic pathways. The differential expressed genes (DEGs) of SARS-COV-2 and lung cancer were explored and were used for protein network and cluster generation. Further function enrichment and gene ontology analysis were performed for all the clusters and were compared between the SARS-COV-2 and lung cancer. The analysis revealed 23 common genes and important pathways involved in tumor immune evasion, cancer proliferation, and immune signaling mainly; T cell signaling, IL- 2& IL-4 signaling, interferon signaling, and chemokine signaling pathways. From the common genes identified, biomarkers were obtained; FHL1, CENPE, PAK2, CASP4, FGF2, and SHC2 through overall survival analysis and immune cell infiltration analysis. These findings suggest that SARS-CoV-2 can play a significant role in cancer relapse by supporting tumorigenic conditions in the tumor microenvironment and facilitating tumor cell migration.