PRDM15 (PR/SET Domain 15)

This study demonstrated that PRDM15 in GC cells could recruits the histone methyltransferase complex PRMT5/Mep50/WDR5 to promote PVR transcription, thereby activating the PVR/TIGIT axis, which inhibits TRM cells activation and mediates immune escape and GC progression.

Furthermore, PRDM15 depletion enhances the sensitivity of HCT116 cells to the chemotherapeutic agent 5-Fluorouracil (5-FU). Mechanistically, PRDM15 functions as a novel negative regulator of p53, exerting its oncogenic effects by transcriptionally downregulating USP10, which in turn destabilizes p53. These findings underscore the critical role of the PRDM15-USP10-p53 axis in CRC progression, offering new insights into the molecular mechanisms driving CRC and identifying potential therapeutic targets for intervention.

This study describes a novel METTL16-PRDM15-FGFR4 signaling axis which is crucial for CCA growth and may have important therapeutic implications. We showed that depletion of METTL16 significantly inhibited CCA cell proliferation and decreased tumor progression.

Our findings revealed that inhibiting PRDM15 was potent to overcome radioresistance through abrogating DNA repair in colorectal cancer cells. Additionally, the expression level of PRDM15 could be applied to predict radiotherapy responsiveness and the outcome of neoadjuvant radiotherapy in rectal cancer patients.

To evaluate the prognostic significance of these 4 signatures, we performed signature recovery on two independent FL datasets annotated with mature clinical data (both with OS, one with failure free survival (FFS), which identified heterogeneous survival outcomes between transcriptional subtypes (Figure 1) and highlighted the potential predictive value of the signatures for treatment naïve patients initiating frontline therapy with rituximab and chemotherapy...In summary, our analyses uncovered genetic subtypes of FL with distinct biological and clinical features, providing a potential framework for advancing precision medicine strategies in FL. These results suggest the possibility of using transcriptional signatures and/or their surrogates as novel biomarkers to guide front-line risk-adapted therapy.