PRPF3 (Pre-MRNA Processing Factor 3)

Further explorative analysis showed that this transcript correlated with the alternative splicing of genes involved in RNA binding and mitochondrial protein synthesis. Overall, our study, for the first time, revealed the association patterns of splicing factor transcripts over time in CRC, identified a transcript of PRPF38A as a candidate late-outcome marker, and provided mechanistic insights into outcome heterogeneity in CRC.

PRPF4 knockdown inhibits GBM progression by reducing p38 MAPK and ERK signaling cascade with metabolic alterations. Targeting PRPF4 may offer novel therapeutic strategies for GBM treatment.

This study provides a comprehensive analysis of the epigenetic landscape in HCC, encompassing both chromatin accessibility and the transcriptome. Our findings reveal that ZNF93 promotes the proliferation and motility of HCC cells through transcriptional regulation of a novel oncogene, PRPF3.

Transcriptome analysis and experimental validations revealed that Prpf31 deficiency extensively perturbed the alternative splicing of mitosis-related genes. Collectively, our findings elucidate a previously undescribed role for Prpf31 in HSPC expansion, through regulating the alternative splicing of mitosis-related genes.