Electronic Journal of Biotechnology

Systems-level analysis prioritizes the importance of IFNG, SULF1, and OAS3 genes in head and neck cancer

2026-03-17T13:39:29+00:00

Background: Head and neck cancer (HNC) is one of the most prevalent and challenging diseases affecting a 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.

Results: 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^−DDC_T) 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.

Conclusions: A substantial correlation between the pathophysiology of HNC and the IFNG, SULF1, and OAS3 genes is found. This research could expedite the progress of drug discovery and aid in modifying HNC’s treatment approaches.

Exploring the molecular mechanism of resveratrol for the treatment of lung adenocarcinoma based on molecular docking

2026-03-17T14:14:01+00:00

Background: Resveratrol (RES) has been found to inhibit the progression of lung cancer. Our study aims to explore the molecular mechanisms by which RES regulates lung adenocarcinoma (LUAD) progression.

Results: Our study unveils two key novel findings: First, our study demonstrates that EPHB2 is a direct functional target of RES in LUAD. Molecular docking and CETSA confirmed the binding, and crucially, EPHB2 overexpression reversed the anti-tumor effects of RES. Second, our study reveals a previously unrecognized role for EPHB2 in promoting glycolysis in LUAD, which is effectively suppressed by RES. Specifically, RES potently inhibited LUAD tumor growth in vivo and suppressed cell proliferation, migration, invasion, and glycolysis in vitro. These inhibitory effects were consistently abolished upon EPHB2 overexpression.

Conclusions: Collectively, our findings suggest that RES inhibits LUAD cell proliferation, migration, invasion, and glycolysis, with EPHB2 downregulation appearing to contribute to these effects. Further studies are needed to determine whether RES directly targets EPHB2 and to evaluate the translational potential of these findings.

AKT/p65-dependent upregulation of CD64 by LPS drives pathogenesis and diagnostic potential in sepsis

2026-03-17T15:31:42+00:00

Background: Sepsis is a life-threatening condition characterized by organ dysfunction caused by a dysregulated host response to infection. Despite improvements in clinical management, both incidence and mortality remain high. Identifying biomarkers with high sensitivity and specificity is critical for early diagnosis. CD64, an Fcγ receptor upregulated on neutrophils during infection, has emerged as a promising diagnostic indicator. This study aimed to evaluate the diagnostic and mechanistic role of CD64 in pediatric sepsis.

Results: A total of 200 children with sepsis and 166 healthy controls were enrolled. At a cutoff value of 0.165, the CD64 index achieved a diagnostic sensitivity of 87.0% and specificity of 92.8%, outperforming conventional markers such as procalcitonin (PCT), C-reactive protein (CRP), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Mechanistic assays demonstrated that lipopolysaccharide (LPS) stimulation induced CD64 expression through the Protein Kinase B (AKT) signaling pathway. Both LPS exposure and AKT overexpression promoted p65 nuclear translocation, and chromatin immunoprecipitation confirmed p65 binding to the CD64 promoter, thereby enhancing CD64 transcription.

Conclusions: CD64 exhibits superior diagnostic and prognostic performance compared to traditional inflammatory markers and serves as a reliable biomarker for pediatric sepsis. Mechanistically, CD64 upregulation is mediated by the AKT/p65 signaling axis. These findings provide a foundation for integrating CD64 into early diagnostic workflows and developing targeted therapeutic strategies in sepsis management.