Abstract
Alternative splicing (AS) plays a crucial role in regulating gene expression and protein diversity, influencing both normal cellular function and pathological conditions, including cancer. Protein pre-mRNA processing factor 8 (PRPF8), a core component of the spliceosome, is integral to the splicing process, ensuring accurate gene transcription and spliceosome assembly. Disruptions in PRPF8 function are linked to a variety of cancers, as mutations in this gene can induce abnormal splicing events that contribute to tumorigenesis, metastasis, and drug resistance. This review provides an in-depth analysis of the mechanisms by which PRPF8 regulates tumorigenesis through AS, exploring its role in diverse cancer types, including breast, liver, myeloid, and colorectal cancers. Furthermore, we examine the molecular pathways associated with PRPF8 dysregulation and their impact on cancer progression. We also discuss the emerging potential of targeting PRPF8 in cancer therapy, highlighting challenges in drug development.