Background: COVID-19, the current global pandemic caused by SARS-CoV-2 infection, can damage the heart and lead to heart failure (HF) and even cardiac death. The 2',5'-oligoadenylate synthetase (OAS) gene family encode interferon (IFN)-induced antiviral proteins which is associated with the antiviral immune responses of COVID-19. While the potential association of OAS gene family with cardiac injury and failure in COVID-19 has not been determined. Methods: The expression levels and biological functions of OAS gene family in SARS-CoV-2 infected cardiomyocytes dataset (GSE150392) and HF dataset (GSE120852) were determined by comprehensive bioinformatic analysis and experimental validation. The associated microRNAs (miRNAs) were explored from Targetscan and GSE104150. The potential OAS gene family-regulatory chemicals or ingredients were predicted using Comparative Toxicogenomics Database (CTD) and SymMap database. Results: The OAS genes were highly expressed in both SARS-CoV-2 infected cardiomyocytes and failing hearts. The differentially expressed genes (DEGs) in the two datasets were enriched in both cardiovascular disease and COVID-19 related pathways. The miRNAs-target analysis indicated that 10 miRNAs could increase the expression of OAS genes. A variety of chemicals or ingredients were predicted regulating the expression of OAS gene family especially estradiol. Conclusion: OAS gene family is an important mediator of HF in COVID-19 and may serve as a potential therapeutic target for cardiac injury and HF in COVID-19.

Background: OAS gene family plays an important role in antiviral process, but its role in pancreatic cancer has not yet been studied. Methods: We analyzed the expression, prognostic value and biological function of the OAS gene family in human pancreatic cancer through comprehensive bioinformatic analysis and cellular level validation. Results: OAS family was highly expressed in pancreatic cancer, and this high expression significantly affected the clinical stage and prognosis of the tumor. OAS gene family was closely related to the immune infiltration of pancreatic cancer, especially neutrophils and dendritic cells, and many immune-related factors and pathways are enriched in the tumor, such as type I interferon signaling pathway and NOD-like receptor signaling pathway. Conclusion: Taken together, high expression of OAS family is closely related to poor prognosis of pancreatic cancer. OAS gene family may serve as the biomarker and even therapeutic target of pancreatic cancer.

Colorectal cancer (CRC) is one of the malignant tumors with the highest morbidity and mortality and poor prognosis. The mammalian gene family of Cab45/reticulocalbin/ERC-45/calumenin (CREC) consists of RCN1, RCN2, RCN3, SDF4 and CALU. Although CREC family members have been associated with CRC, the expression pattern, prognostic value, and the role of CREC family in CRC remain unclear. In this study, the expression, survival and biological functions of CREC family in CRC were determined via bioinformatic datasets analysis and experimental verification on clinical CRC specimen. Bioinformatic analysis showed that the expression levels of most CREC family genes were higher in CRC tissues than in normal colorectal tissues. The qPCR and western blot results also revealed that the transcriptional and protein levels of CREC family were elevated in CRC tissues compared with adjacent tissues. Besides, CREC family was significantly correlated with advanced tumor stage and poor prognosis of CRC patients. The expression levels of CREC family had correlations with genomic mutation and methylation, and with the infiltration levels of CD4 + T cells, macrophages, neutrophils, and dendritic cells in the microenvironment of CRC. Functional networks enrichment analysis indicated that the genes of CREC family were essential factors for CRC metastasis. Collectively, these findings suggest that CREC family might be potential targets for the treatment of CRC and candidate prognostic markers for CRC patients.

Background: The PLOD gene family, involved in extracellular matrix (ECM) remodeling, plays a role in tumor progression, but its comprehensive role and clinical significance in clear cell renal cell carcinoma (ccRCC) remains unclear.Methods: We integrated multi-omics bioinformatics analyses from public databases (TCGA, GEO) with experimental validation using RT-qPCR, western blotting, and functional assays to systematically evaluate the expression patterns, prognostic value, immune microenvironment associations and drug resistance of PLOD genes in ccRCC. Computational approaches, including the comparative toxicogenomics database and molecular docking, were further employed to identify potential chemical modulators.Results: PLOD1, PLOD2, and PLOD3 were consistently overexpressed at both mRNA and protein levels in ccRCC tissues and cell lines. High PLOD expression was significantly correlated with reduced overall survival, and poor disease-free survival. Functional enrichment analysis revealed the involvement of PLOD gene family in collagen biosynthesis, ECM-receptor interaction, and lysine degradation pathways. PLOD expression was also linked to an immunosuppressive microenvironment and resistance to conventional therapeutics. Through toxicogenomics screening and molecular docking, acetaminophen was identified as a potential regulator of all three PLOD proteins.Conclusions: This study underscores the pivotal role of the PLOD family in ccRCC pathogenesis through ECM remodeling, immune modulation, and therapy resistance. Our results support their utility as diagnostic and prognostic biomarkers, and acetaminophen may serve as a candidate for targeting PLOD-mediated pathways, providing a foundation for future preclinical and therapeutic investigations.