F11R (F11 Receptor)

Our results demonstrated that MEG3 and its potential downstream regulator, F11R could be involved in PDAC progression, particularly in patients with long-DM. The findings underscore the clinical significance of epigenetic regulation in DM-related PDAC, suggesting novel targets such as MEG3 and F11R for potential therapeutic intervention.

F11R regulates EMT and Rap1 signalling, thereby influencing CRC metastasis. Its reduced expression is associated with unfavourable outcomes and tumour progression. Cell type-specific enrichment in endothelial and epithelial cells, along with links to immune subsets, highlights F11R as a potential prognostic biomarker in CRC.

Our findings highlight implications for MDM2 regulation by ADAR1-dependent 3'UTR RNA editing and present an interplay between RNA editing on 3'UTRs and the mRNA polyadenylation machinery. These results improve our understanding of ADAR1's role in cancer-associated 3' UTR RNA editing and its potential as a therapeutic target.

Further analyses suggested that PPIF up-regulation in Macrophage-C1-C1QC cells was associated with the enhancement of their anti-inflammatory phenotype and the promotion of F11R-F11R signaling with malignant cells, allowing LSCC cells to evade macrophage-mediated cytotoxicity. Our study provides new insights into the cellular dynamics of LSCC and highlights the critical role of Macrophage-C1-C1QC and PPIF in LSCC progression, offering potential therapeutic targets for treatment.

These findings suggest that VCAN-AS1 facilitates GC progression through the HuR/F11R pathway, offering new insights into GC pathogenesis and identifying VCAN-AS1 as a potential therapeutic target for GC treatment.

Although molecularly targeted therapies have shown efficacy in other hematologic malignancies, currently venetoclax is the only targeted therapy approved for MM (t(11;14))...It addresses gene therapies, small molecule inhibitors and monoclonal antibodies currently under investigation to antagonize oncogenic drivers including MCL-1, BCL9, F11R, and CKS1B, all of which are implicated in cell survival, proliferation or drug resistance. In conclusion, the link between chromosome 1 abnormalities and high-risk disease in MM patients offers a compelling rationale to identify and explore therapeutic targeting of chromosome 1 gene products as a novel precision medicine approach for a poorly served patient population.

Lastly, we show capture of orthogonal phagocytic surfaceomes across different cells, using a neutrophil-like model. We believe this method will enable new insights into phagocytic processes in a variety of contexts.

This study explored the UBE2I gene as a potential biomarker in OC and EC. Further, this study concludes that the irinotecan hydrochloride drug has higher therapeutic effects on UBE2I protein through docking and dynamics studies.

In vitro experiments verified that JAM-A knockdown suppressed the proliferation and migration abilities of breast cancer cells and liver cancer cells. Overall, our study suggests that JAM-A is a pan-cancer regulator and a potential biomarker for predicting prognosis and immune-therapeutic responses for different tumors.

Moreover, the F11R trinucleotide editing showed promising predictive performance for diagnosing GC and CRC across GC and CRC cohorts. Our findings thus highlight both the potential biological and clinical significance of an ADAR-edited F11R trinucleotide in GC and CRC, providing new insights into its application as a novel diagnostic biomarker for both cancers.

Our bioinformatic study revealed that FYN, INADL, OCLN, F11R, and TOP2A were potential biomarker panel of BCSCs from secretome.

By exploring genes commonly identified in the both analyses, F11R and PTGIR were characterized as membrane markers in CTCs of mesenchymal state in breast cancer, which were evaluated by enriched terms, literature evidence, and relevant molecular pathways. We expect that the results will be helpful to more effective strategies for metastasis management.