Differentially Expressed Genes in Lung Cancer: Molecular Docking of Hypoxanthine Guanine-Phosphoribosyl Transferase with Dibutyl Phthalate

This study aimed to identify differentially expressed genes (DEGs) by molecular docking of the hypoxanthine guanine-phosphoribosyl transferase (HGPRT) protein with pulmonary toxins i.e., dibutyl phthalate (DBP) and its metabolites, responsible for the induction of lung cancer. The highest binding affinity of −7.0 kcal/mol obtained was of monobutyl phthalate acyl-A-D-glucuronide. DBP and the protein HGPRT have a strong binding affinity of −7.0 kcal/mol, indicating the possibility of interrupting important biochemical pathways in the treatment of lung cancer. The development of targeted medicines may be guided by this relationship. A total of 120 samples were obtained from the GSE19804 expression profile out of which 60 samples from lung cancer and 60 from normal patients were selected as experimental and control groups. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses elaborated that the gene is involved in purine metabolism, nucleotide metabolism, drug metabolism and the synthesis of several enzymes. The protein–protein interaction (PPI) was assessed using the Search Tool for the Retrieval of Interacting Genes (STRING) database using Cytoscape software. The PPI enrichment [Formula: see text]-value was obtained as <1.0e−16. The docking result of the protein encoded by the AGER gene with DBP was obtained with a minimum binding affinity of up to −6.8 kcal/mol. The soluble receptor for advanced glycation end-products (sRAGE) was found to be involved in inhibiting the activation of oxidative stress and apoptotic pathways. Lung cancer is mostly dependent on the AGER gene and its soluble receptor sRAGE. sRAGE functions as a ruse to counteract the pro-inflammatory effects of AGER signaling and may be a therapeutic target to slow the growth of the malignancy. This study lays the framework for future research and offers novel insights into the role of HGPRT and DBP in the development of lung cancer and targeted therapy.