OASL (2'-5'-Oligoadenylate Synthetase Like)

In contrast, the bursa exhibited persistent modulation of colipase (CLPS), chymotrypsinogen B1 (CTRB1), and deoxyribonuclease I (DNASE1), indicating metabolic and apoptotic remodeling. These results demonstrate that in ovo mRNA vaccination against MDV rapidly activates organ-specific immune and metabolic pathways, providing a transcriptomic framework for the rational design of poultry mRNA vaccines.

OASL promotes HCC progression by inhibiting the cGAS-STING pathway, sustaining high matrix stiffness, and suppressing M1 macrophage polarization. Targeting OASL may offer a novel therapeutic strategy to remodel TME stiffness and restore anti-tumor immunity in HCC.

Results show that OASL regulates OXA-induced ICD in GC cells via the cGAS-STING pathway, impacting chemosensitivity. The findings suggest new targets and strategies for improving GC therapy by modulating OASL expression to enhance OXA sensitivity through ICD mechanisms.

KEGG analysis revealed that DEGs were involved in signal pathways such as combined proteoglycan interaction, glycoprotein hormone and peptide hormone biosynthesis, non-integrin membrane-extracellular matrix interaction, and protein digestion and absorption, and the top 20 key genes of GC were identified, including OASL, ISG20, RAB3A, CREM, BIRC7, LHB, etc. FGL1 is a potential biomarker for the diagnosis and prognosis of GC. FGL1-mediated signaling pathways may be a new target for GC therapy in future.

Drug prediction and molecular docking identified chlorendic acid, idarubicin, PHA-848,125, and tosedostat as potential activators of the OAS family due to their strong binding affinity. Conversely, GW842166, NSC 23,766, and metolazone showed high binding affinity for OASL and may inhibit its expression. In summary, The OAS gene family, associated with poor prognosis in gastric cancer, promotes tumour progression and represents a promising therapeutic target.

These findings were further corroborated by our single-cell RNA data and multiplex immunohistochemistry results, which provided additional substantiation for the observed interactions. These observations regarding the interaction between the tumor microenvironment and nasopharyngeal carcinoma have significant clinical implications for the future treatment of NPC.

These results not only reveal the antiviral role of CSF3 but also provide new insights into the host's innate immune response to ALV. Furthermore, they highlight the potential of CSF3 as a candidate resistance gene for breeding programs or as a vaccine adjuvant for disease prevention.

Our results highlight the importance of a combinational strategy employing both epigenetic and immunotherapy in HNSCC.

Using both loss- and gain-of-function studies, we find that OASL reprograms FA metabolism to enhance oncogenesis, which can be inhibited by an FA synthesis inhibitor. Our results define OASL as an important factor in regulating mRNA translation, mediating tumor-promoting functions of IFN-Is, and providing potential therapeutic interventions.

TYMS was a hub gene in the prognostic signature, and was strongly associated with LUAD progression and cell proliferation in the experimental validation. The lung TRM cell-related prognostic signature is an effective tool for predicting the prognosis and therapeutic outcomes of patients with LUAD.

These findings suggest that butyrate supports a beneficial antiviral response in host cells during FAdV-4 infection. This study provides the role of SCFAs in modulating host defense mechanisms against avian viral infections.

Single-cell sequencing of CD45+ cells reveals that HTR2B activation enhances the production of OASL1+ macrophages, contributing to the observed enhancement of antitumor immunity. These findings propose HTR2B as a novel therapeutic target for treating osteosarcoma, offering a dual mechanism of action that directly impedes tumor cell proliferation and augments the host immune response.