Bud31, also known as Functional Spliceosome-Associated Protein 17, is a spliceosome component. It is involved in pre-mRNA splicing and processing, and acts as a transcriptional regulator of androgen receptor (AR) target genes [3,5,6]. It plays a crucial role in multiple biological processes, with its function being closely related to cell cycle regulation, cell differentiation, and cancer development [3,4]. Genetic models, especially KO/CKO mouse models, have been valuable in studying its functions.

In mice, germ cell-specific knockout of Bud31 led to loss of spermatogonia and male infertility, indicating its requirement for spermatogonial stem cell pool maintenance and the initiation of spermatogenesis. Deletion of Bud31 in germ cells caused widespread exon-skipping and intron retention, for example, resulting in retention of the first intron of Cdk2 and a decrease in Cdk2 expression [1]. In ovarian cancer, knockdown of Bud31 promoted exon 3 skipping of BCL2L12, leading to a truncated isoform that underwent nonsense-mediated mRNA decay and subsequent apoptosis of cancer cells [2]. In clear cell renal cell carcinoma (ccRCC), BUD31 knockdown inhibited cell proliferation, migration, and invasion in vitro and reduced tumor growth in vivo, and RNA sequencing identified 390 alternative splicing events regulated by BUD31, including 17 cell cycle-related genes [4]. In prostate cancer cell lines, knockdown of BUD31 promoted cell proliferation and migration via activation of p-AKT and vimentin [3].

In conclusion, Bud31 is essential for processes such as spermatogenesis and has significant implications in cancer development. Studies using KO/CKO mouse models have revealed its role in regulating alternative splicing, which impacts cell-related functions in spermatogonial stem cells and cancer cells, providing insights into potential therapeutic targets for male infertility and various cancers.