Matches in SemOpenAlex for { <https://semopenalex.org/work/W4307138768> ?p ?o ?g. }
- W4307138768 abstract "Abstract Dysregulated expression of splicing factors has important roles in cancer development and progression. However, it remains a challenge to identify the cancer-specific splicing variants. Here we demonstrate that spliceosome component BUD31 is increased in ovarian cancer, and its higher expression predicts worse prognosis. We characterize the BUD31-binding motif and find that BUD31 preferentially binds exon-intron regions near splicing sites. Further analysis reveals that BUD31 inhibition results in extensive exon skipping and a reduced production of long isoforms containing full coding sequence. In particular, we identify BCL2L12 , an anti-apoptotic BCL2 family member, as one of the functional splicing targets of BUD31. BUD31 stimulates the inclusion of exon 3 to generate full-length BCL2L12 and promotes ovarian cancer progression. Knockdown of BUD31 or splice-switching antisense oligonucleotide treatment promotes exon 3 skipping and results in a truncated isoform of BCL2L12 that undergoes nonsense-mediated mRNA decay, and the cells subsequently undergo apoptosis. Our findings reveal BUD31-regulated exon inclusion as a critical factor for ovarian cancer cell survival and cancer progression." @default.
- W4307138768 created "2022-10-28" @default.
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- W4307138768 date "2022-10-21" @default.
- W4307138768 modified "2023-09-28" @default.
- W4307138768 title "Splicing factor BUD31 promotes ovarian cancer progression through sustaining the expression of anti-apoptotic BCL2L12" @default.
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- W4307138768 doi "https://doi.org/10.1038/s41467-022-34042-w" @default.
- W4307138768 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36271053" @default.
- W4307138768 hasPublicationYear "2022" @default.
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