Identification of genetic associations between acute myocardial infarction and non-small cell lung cancer

A growing body of evidence suggests a potential connection between myocardial infarction (MI) and lung cancer (LC). However, the underlying pathogenesis and molecular mechanisms remain unclear. This research aims to identify common genes and pathways between MI and LC through bioinformatics analysis.

Two public datasets (GSE166780 and GSE8569) were analyzed to identify differentially expressed genes (DEGs). Common DEGs were enriched using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Hub genes were identified and their diagnostic performance was evaluated. Gene co-expression networks, as well as regulatory networks involving miRNA-hub genes and TF-hub genes, were also constructed. Finally, candidate drugs were predicted.

Among the datasets, 34 common trend DEGs were identified. Enrichment analysis linked these DEGs to key biological processes, cellular components, and molecular functions. Eight hub genes (CEBPA, TGFBR2, EZH2, JUNB, JUN, FOS, PLAU, COL1A1) were identified, demonstrating promising diagnostic accuracy. Key transcription factors associated with these hub genes include SP1, ESR1, CREB1, ETS1, NFKB1, and RELA, while key miRNAs include hsa-mir-101-3p, hsa-mir-124-3p, hsa-mir-29c-3p, hsa-mir-93-5p, and hsa-mir-155-5p. Additionally, potential therapeutic drugs were identified, with zoledronic acid anhydrous showing potential value in reducing the co-occurrence of the two diseases.

This study identified eight common signature genes shared between NSCLC and AMI. Validation datasets confirmed the diagnostic value of key hub genes COL1A1 and PLAU. These findings suggest that shared hub genes may serve as novel therapeutic targets for patients with both diseases. Ten candidate drugs were predicted, with zoledronic acid showing potential for targeting dual hub genes, offering a promising therapeutic approach for the comorbidity of lung cancer and myocardial infarction.