Early Detection of Biomarkers and Targeted Drug Therapy for Lung and Liver Cancer
Publisher
University of Tennessee at Chattanooga
Place of Publication
Chattanooga (Tenn.)
Abstract
Abstract:
Lung adenocarcinoma (LUAD) and liver hepatocellular carcinoma (LIHC) are among the leading causes of cancer-related mortality worldwide and are often diagnosed at advanced stages due to limited early symptoms and effective biomarkers. To identify shared molecular drivers, four Gene Expression Omnibus (GEO) datasets were analyzed to detect common differentially expressed genes (DEGs) between LUAD and LIHC. A total of 21 overlapping DEGs were identified. Protein–protein interaction (PPI) network analysis revealed strong interaction clusters centered on SPP1 and COL1A1, which were further confirmed as hub genes using CytoHubba. Reactome pathway enrichment analysis demonstrated that these genes are primarily involved in extracellular matrix (ECM) remodeling, cell adhesion, migration, and immune-related pathways associated with tumor progression and metastasis.
Survival and expression analyses using UALCAN showed that high SPP1 expression correlates with poor overall survival in LIHC and is significantly elevated in both LUAD and LIHC tumor tissues. To explore therapeutic potential, molecular docking studies were performed. Ligands were prepared by removing water molecules and optimizing charges and hydrogen atoms. Among tested compounds, Tretinoin exhibited the strongest binding affinity with SPP1 (−7.6 kcal/mol), exceeding the ideal threshold of −5 kcal/mol. Interaction analysis using BIOVIA Discovery Studio revealed stable hydrogen bonding, alkyl, and π-alkyl interactions between SPP1 and Tretinoin.
These findings suggest that SPP1 and COL1A1 serve as shared oncogenic drivers in LUAD and LIHC. In particular, SPP1 may function as a prognostic biomarker and a potential therapeutic target. Further experimental validation is warranted to confirm gene expression patterns and to investigate the therapeutic efficacy of the SPP1–Tretinoin interaction.
Document Type
abstracts (summaries)
Language
English
Rights
http://rightsstatements.org/vocab/InC/1.0/
License
http://creativecommons.org/licenses/by/4.0/
Recommended Citation
Meeks, Shelby; Smith, Samuel; and Ferdoush, Jannatul, "Early Detection of Biomarkers and Targeted Drug Therapy for Lung and Liver Cancer". ReSEARCH Dialogues Conference proceedings. https://scholar.utc.edu/research-dialogues/2026/presentations/6.
Early Detection of Biomarkers and Targeted Drug Therapy for Lung and Liver Cancer
Abstract:
Lung adenocarcinoma (LUAD) and liver hepatocellular carcinoma (LIHC) are among the leading causes of cancer-related mortality worldwide and are often diagnosed at advanced stages due to limited early symptoms and effective biomarkers. To identify shared molecular drivers, four Gene Expression Omnibus (GEO) datasets were analyzed to detect common differentially expressed genes (DEGs) between LUAD and LIHC. A total of 21 overlapping DEGs were identified. Protein–protein interaction (PPI) network analysis revealed strong interaction clusters centered on SPP1 and COL1A1, which were further confirmed as hub genes using CytoHubba. Reactome pathway enrichment analysis demonstrated that these genes are primarily involved in extracellular matrix (ECM) remodeling, cell adhesion, migration, and immune-related pathways associated with tumor progression and metastasis.
Survival and expression analyses using UALCAN showed that high SPP1 expression correlates with poor overall survival in LIHC and is significantly elevated in both LUAD and LIHC tumor tissues. To explore therapeutic potential, molecular docking studies were performed. Ligands were prepared by removing water molecules and optimizing charges and hydrogen atoms. Among tested compounds, Tretinoin exhibited the strongest binding affinity with SPP1 (−7.6 kcal/mol), exceeding the ideal threshold of −5 kcal/mol. Interaction analysis using BIOVIA Discovery Studio revealed stable hydrogen bonding, alkyl, and π-alkyl interactions between SPP1 and Tretinoin.
These findings suggest that SPP1 and COL1A1 serve as shared oncogenic drivers in LUAD and LIHC. In particular, SPP1 may function as a prognostic biomarker and a potential therapeutic target. Further experimental validation is warranted to confirm gene expression patterns and to investigate the therapeutic efficacy of the SPP1–Tretinoin interaction.