GPRC5A (G Protein-Coupled Receptor Class C Group 5 Member A)

Our findings indicated that the rondom froest model based on five autoantibodies might help identify preclinical and early-stage PC.

Furthermore, NK92 cell-derived exosomes effectively delivered ABCB1 siRNA into recipient cells, mediating efficient gene silencing to sensitize chemoresistant ovarian cancer cells to therapeutic agents. Overall, this study provides a novel strategy to treat ovarian cancer through the preparation of genetically modified NK92 cell-derived exosomes loaded with RNA interference.

Conclusions : This study identifies TICs as the developmental origin of neoplastic stem-like states and delineates early transcriptional and pathway reprogramming events that drive the transition from normal to premalignant colonic epithelium. These findings provide new insight into CRC initiation and nominate biomarkers with translational potential for early detection and therapeutic targeting.

This study provides new insights into the endocytic mechanisms of GPRC5A, for which no specific ligand has been identified to date. Further research may uncover additional Gal-3-mediated functions in GPRC5A cellular signaling and contribute to the development of innovative therapeutic strategies.

These findings were confirmed using primary CAFs and NFs models. Our study unveils GPRC5A as a key mediator in ESCC and proposes the GPRC5A/TGF-β/ANXA1 axis as a promising therapeutic target for ESCC treatment.

This study highlights the potential of GPD2 and the glycolysis-related gene signature as prognostic biomarkers and therapeutic targets in CCA. The signature offers insights into tumor biology, immune interactions, and potential personalized treatment strategies, paving the way for improved management of this aggressive cancer.

An interactive web portal to explore the full results and visualizations is available at pc-biomarkers.de. Future work will further validate these biomarkers to improve early detection, prognosis, and treatment strategies.

This study proposes a glycolysis assessment strategy based on the interquartile range, which effectively addresses the limitations of previous scoring methods, including insufficient resolution and limited robustness. The proposed method enables more accurate quantification of intracellular glycolysis levels and facilitates fine-grained characterization of metabolic states. Furthermore, it identifies GPRC5A as a potential biomarker for the early diagnosis of gastric cancer. These findings enhance our understanding of metabolic reprogramming in gastric cancer and provide support for targeting the glycolytic pathway in therapeutic interventions.

In vivo studies confirmed that GPRC5A silencing reduced tumor growth and improved survival, highlighting its potential as a therapeutic target for overcoming chemoresistance in GBM. These findings underscore the critical role of GPRC5A in GBM and suggest that targeting the GPRC5A-GLUT1 interaction could improve patient outcomes.

The GPRC5A-CXCL8-NET-cfDNA axis has a critical role in the development of therapeutic resistance to GnP in PDAC. Targeting this axis may represent a promising strategy for overcoming GnP resistance and thereby enhancing the efficacy of chemotherapy in PDAC.

Proteogenomic analysis is applied to samples from the CALGB 40601 (Alliance) randomized neoadjuvant trial of trastuzumab, lapatinib, or the combination to identify biomarkers associated with pathological response status. Thus, proteogenomic analysis identifies negative biomarkers for pCR and alternative plasma membrane targets for treatment-resistant HER2+ breast cancer. This trial is registered at clinicaltrials.gov (NCT00770809).

In conclusion, both VD and RA stimulate GPRC5A expression. The mechanisms involve a common and essential PKC signalling pathway, as Gö6983 inhibited both VD- and RA-induced signalling.