BUD31 is a spliceosomal component protein that functions primarily in pre-mRNA splicing and alternative splicing regulation 1. Structurally, BUD31 localizes to the B complex stage of spliceosome assembly and participates in 5' splice site recognition and exon binding 2. Beyond splicing, BUD31 acts as a transcriptional coactivator of androgen receptor (AR) target genes, increasing AR transactivation through direct protein-peptide interactions 3. In cancer biology, BUD31 dysregulation drives multiple malignancies. In ovarian cancer, elevated BUD31 expression promotes cancer progression by regulating exon inclusion in the anti-apoptotic gene BCL2L12, sustaining cancer cell survival 4. In MYC-driven cancers, BUD31 becomes a synthetic lethal target because MYC hyperactivation increases precursor mRNA synthesis, creating heightened splicing burden that partial spliceosome inhibition exploits selectively 5. High BUD31 expression correlates with worse prognosis in clear cell renal cell carcinoma and prostate cancer, promoting cell cycle progression and cell migration through alternative splicing of cell cycle-related genes 67. Clinically, BUD31 represents a therapeutic target. Antisense oligonucleotides inducing BCL2L12 exon skipping promote apoptosis in ovarian cancer cells 4, suggesting direct therapeutic utility. BUD31 serves as an independent prognostic biomarker for poor outcomes across multiple cancers, warranting investigation as both a diagnostic and therapeutic target 8.