Identification of Key Hub Genes in Lung and Esophageal Cancer for Potential Therapeutic Interventions
Publisher
University of Tennessee at Chattanooga
Place of Publication
Chattanooga (Tenn.)
Abstract
Abstract: Non-small cell lung cancer (NSCLC) and esophageal squamous cell carcinoma (ESCC) are leading causes of cancer-related mortality worldwide. Although they arise in distinct tissues, these malignancies may share common molecular mechanisms that drive tumor progression and metastasis. This study aimed to identify shared oncogenic drivers and potential therapeutic targets using an integrated bioinformatics approach.
Four Gene Expression Omnibus (GEO) datasets were analyzed to identify differentially expressed genes (DEGs) common to both NSCLC and ESCC. Protein–protein interaction (PPI) network analysis was performed to determine hub genes, and their clinical relevance was validated using The Cancer Genome Atlas (TCGA) database. Functional enrichment analysis was conducted to explore associated biological pathways, followed by molecular docking to evaluate potential therapeutic interactions.
Thirty-nine DEGs were consistently dysregulated across both cancer types. Among them, MMP1 emerged as a central hub gene and was significantly upregulated in tumor tissues. Functional enrichment analysis revealed that these genes are primarily involved in extracellular matrix (ECM) organization and remodeling pathways, highlighting their role in tumor invasion and metastasis. As a matrix-degrading enzyme, MMP1 promotes extracellular matrix breakdown, facilitating cancer cell migration and metastatic spread. Molecular docking analysis demonstrated strong predicted binding affinity between MMP1 and leflunomide, an immunomodulatory drug that inhibits cell proliferation by blocking pyrimidine synthesis.
Collectively, these findings identify MMP1 as a promising prognostic biomarker and potential therapeutic target in both NSCLC and ESCC. Future studies will focus on experimental validation in patient samples, mechanistic investigations, and in vitro and in vivo evaluation of MMP1-targeted therapeutic strategies.
Document Type
abstracts (summaries)
Language
English
Rights
http://rightsstatements.org/vocab/InC/1.0/
License
http://creativecommons.org/licenses/by/4.0/
Recommended Citation
Davis, Emma; Smith, Samuel; and Ferdoush, Jannatul, "Identification of Key Hub Genes in Lung and Esophageal Cancer for Potential Therapeutic Interventions". ReSEARCH Dialogues Conference proceedings. https://scholar.utc.edu/research-dialogues/2026/presentations/8.
Identification of Key Hub Genes in Lung and Esophageal Cancer for Potential Therapeutic Interventions
Abstract: Non-small cell lung cancer (NSCLC) and esophageal squamous cell carcinoma (ESCC) are leading causes of cancer-related mortality worldwide. Although they arise in distinct tissues, these malignancies may share common molecular mechanisms that drive tumor progression and metastasis. This study aimed to identify shared oncogenic drivers and potential therapeutic targets using an integrated bioinformatics approach.
Four Gene Expression Omnibus (GEO) datasets were analyzed to identify differentially expressed genes (DEGs) common to both NSCLC and ESCC. Protein–protein interaction (PPI) network analysis was performed to determine hub genes, and their clinical relevance was validated using The Cancer Genome Atlas (TCGA) database. Functional enrichment analysis was conducted to explore associated biological pathways, followed by molecular docking to evaluate potential therapeutic interactions.
Thirty-nine DEGs were consistently dysregulated across both cancer types. Among them, MMP1 emerged as a central hub gene and was significantly upregulated in tumor tissues. Functional enrichment analysis revealed that these genes are primarily involved in extracellular matrix (ECM) organization and remodeling pathways, highlighting their role in tumor invasion and metastasis. As a matrix-degrading enzyme, MMP1 promotes extracellular matrix breakdown, facilitating cancer cell migration and metastatic spread. Molecular docking analysis demonstrated strong predicted binding affinity between MMP1 and leflunomide, an immunomodulatory drug that inhibits cell proliferation by blocking pyrimidine synthesis.
Collectively, these findings identify MMP1 as a promising prognostic biomarker and potential therapeutic target in both NSCLC and ESCC. Future studies will focus on experimental validation in patient samples, mechanistic investigations, and in vitro and in vivo evaluation of MMP1-targeted therapeutic strategies.