Head and neck cancer (HNC) is one of the most prevalent and challenging disease affecting large population worldwide. Functional genomics can help understand the disease, but expressed gene therapy is uncertain. The study sought to identify specific genetic mutations and protein expression profiles in HNC. We ranked IFNG, SULF1, and OAS3 as three HNC-related genes ( p < 0.05) based on the data mining. N-acetyleglucosamine-6-sulfatase activity, arylsulfatase, 2,5-oligoadenylate synthetase activity, interferon-gamma receptor binding, and other essential biological processes were all significantly correlated with the gene ontology (GO) terms. Nucleotide excision repair pathways, RNA polymerase-I transcription start and termination, RNA polymerase-II promoter escape, pyrimidine biosynthesis, and interferon-gamma signaling were all linked in the pathway enrichment. OAS1, IFIT1, CD4, STAT3, NFKBIA, RIPK1, SLCO5A1, and others are functionally connected to the co-expressed genes, while COL3A1 and SCEL are indirectly linked. Compared to controls, the quantitative PCR (qPCR) of these genes showed a significant two-fold change (FC) expression (2−DDCT) pattern of SULF1 (FC ≤ 1.2), OAS3 (FC ≤ 0.13), and IFNG (FC ≤ 0.12) compared to reference gene GAPDH (FC = 1). Pathophysiological cancer development is associated with up- and downregulated expression of these genes. The study found that personalized medicine can improve HNC treatment by adapting medication to each patient’s tumor’s molecular traits. A substantial correlation between the pathophysiology of HNC with the IFNG, SULF1 , and OAS3 genes is fond. This research could expedite the progress of drug discovery and aid in modifying HNC’s treatment approaches.
Khawar et al. (Sun,) studied this question.