PTGDR (Prostaglandin D2 Receptor 2)

This study demonstrates that tumor-specific DNA methylation changes, particularly when evaluated using multi-gene panels can enhance prognostic stratification in GC. These findings support the potential use of methylation-based biomarkers for personalized management of GC.

CS alleviates COPD symptoms by suppressing inflammation, apoptosis, and oxidative stress, suggesting novel therapeutic strategies.

Mechanistically, the enhanced production of IL-1β by Ptgdr-/- DCs contributes to the activation and accumulation of γδ T cells in tumor tissue. In summary, our findings highlight the effectiveness of targeting the PLA2G2D-PGD2/PTGDR axis to reprogram aging dendritic cells, thereby inhibiting melanoma progression and presenting a promising therapeutic target, particularly for elderly patients.

NRG was proved to be an accurate predictor of CRC prognosis. Furthermore, the novel signature exhibited consistent value and translational potential for predicting prognosis, tumor immunogenicity, and therapeutic response in CRC.

These findings were further supported by RT-qPCR and immunofluorescence data, which confirmed the downregulation of PTGDS and PTGDR in LUAD tumor tissues compared to normal tissues. Collectively, these results suggest that PGD2 and its signaling axis play a significant role in tumor-suppressive and anti-inflammatory effects in LUAD, with potential applications in prognosis management and therapy decision-making.

In summary, this study indicated that PGD2/PTGDR2 signaling affects stemness and autophagy in GCSCs. The results suggest that PGD2/PTGDR2 signaling may affect the stemness of GCSCs by regulating autophagy.

Moreover, PTGDR2 knockdown blocked the activation of autophagy by PGD2 and the level of ATG4B ubiquitination in GCSCs. In summary, it was elucidated that the PGD2/PTGDR2 signaling cascade affects GCSCs stemness by regulating autophagy, suggesting that the PGD2/PTGDR2 signaling pathway could serve as a novel target for cancer therapy.

Additionally, reduced PGD2 expression has been associated with poor prognosis in patients with gastric, breast, lung, and pancreatic cancers, validating the preclinical findings and their clinical relevance. This review focuses on the current understanding of PGD2/PTGDR2 expression patterns and biological activity in cancer, proposing questions to guide the assessment of PGD2 and its receptors as potential targets for effective cancer therapies.

DCC methylation in saliva samples could be a non-invasive and efficient tool for early detection of hypopharyngeal cancer in high-risk patients.

The dots represent the observed logFC, the horizontal line the bootstrapped 95%Confidence Intervals; PTGDR2= prostaglandin D2 receptor 2; ns= not significant B) Differentially expressed genes in Non Responders vs Responders CD8pos naïve T cells. FDR=False Discovery Rate; CCL5= Chemokine (C-C motif) ligand 5; PRDM1= PR/SET Domain 1; SGK1= serum/glucocorticoid regulated kinase 1.

Our data suggest that PGD2 may be an important marker and potential therapeutic target in the clinical management of GC. L-PTGDS/PTGDR2 may be one of the critical targets for GC therapy. The PGD2/PTGDR2 signal affects the viability, invasion, apoptosis, and stemness of GCSCs and prevents the progression of GC.

In hypopharyngeal cancer patients, salivary DNA methylation analysis of DCC showed high diagnostic accuracy even at the stage of superficial cancer. Saliva can be collected easily and noninvasively, and could be a useful tool for picking up patients who are at high-risk for hypopharyngeal cancer.