ADORA2B (Adenosine A2b Receptor)

This study identifies ADORA2B as a critical regulator of metastatic progression in UPS, implicating it as a promising therapeutic target. Ongoing clinical trials targeting adenosine pathways further support the translational potential of ADORA2B inhibition to disrupt metastasis and improve outcomes for UPS patients.

Here, we identify that immunosuppressive eADO signaling in the TME is a major barrier to oHSV therapy and CD73 blockade prevents tumor immune escape. The combination of oHSV with CD73 blockade supports the development of an antitumor immune memory response in solid tumors. This study supports clinical development of this combination strategy.

Based on existing evidence, Adora2b regulates epithelial-mesenchymal transition (EMT) in GC cells via the cAMP/PKA/Snail pathway, and preclinical studies show that targeting Adora2b reduces the migration and invasion of GC cells. These findings suggest that targeting Adora2b may provide new insights for gastric cancer therapy.

NM-105 caused hypermethylation, unlike the other TiO2NPs. This study highlights DNA methylation relevance in assessing NMs' toxicity.

The selective HTR2A receptor antagonist ketanserin has the potential to alleviate this toxicological impact. Our study presents an efficient, cost-effective toxicological analysis using network toxicology, offering new insights into dioxin-associated liposarcoma.

Low-risk patients were enriched in fatty acid metabolism and peroxisome pathways, exhibited higher immunotherapy responsiveness, and showed greater sensitivity to Gefitinib and Afatinib. High-risk patients exhibited activation of inflammatory and profibrotic pathways, an elevated TMB, immunosuppressive microenvironments, and greater sensitivity to Topotecan and Irinotecan. RT-qPCR validated the expression of HGRGs across selected cell lines. The prognostic model derived from five HGRGs demonstrates excellent clinical value in predicting prognosis and guiding therapeutic strategies in KIRC.

In conclusion, the hepatoprotective effects of CPT may be related to the suppression of TNF-α-, TLR9-, and ADORA2B-mediated inflammation, oxidative stress, and apoptosis. These results provide a foundation for the development of CPT as a potential therapeutic agent for ALI.

Four SNPs in four genes (ADORA2B, ZFAND2A, APOBEC3B, and PRMT6) were selected and examined for association with susceptibility to GMA. Among the SNPs, rs9435441 in PRMT6 was closely associated with GMA in the minor allele dominant model (p = 0.0004, OR = 2.858). This association could be difficult to identify using an approach based on the known function of PRMT6 because there have been no reports showing direct effects or function of the gene on GMA and/or related conditions. Validation using other populations and experiments to reveal the function of the gene is needed in future studies.

Flow cytometry was used to quantify apoptosis. The results of this investigation validate ADORA2B as a potential therapeutic target and diagnostic biomarker.

This indicates that the regulation of EMT by TC4 is closely associated with its interaction with ADORA2B. The present study confirms that TC4, a newly discovered compound with the ability to inhibit the growth and metastasis of CRC cells, can target ADORA2B to significantly regulate EMT in cancer cells.

ADORA2B is a key oncogenic driver in HNSC, contributing to tumor proliferation, migration, and an immunosuppressive TME. Its high expression is associated with poor prognosis and reduced immunotherapy efficacy. Targeting ADORA2B may enhance therapeutic outcomes and overcome treatment resistance, highlighting its potential as a diagnostic, prognostic, and therapeutic biomarker.

Doxorubicin (DOX), a chemotherapeutic drug used for cancer treatment, faces limitations in clinical use due to its cardiotoxicity...MiR-27b-3p negatively regulated the expression of four target genes (Plk2, Adora2b, Apaf1 and Nrk) in DOX-stimulated cardiomyocytes. In conclusion, miR-27b-3p ameliorates DOX-induced cardiac dysfunction and myocardial injury by inhibiting inflammation and oxidative stress.