Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function - PubMed
5 hours ago
- #splice-switching
- #mitochondrial function
- #ovarian cancer
- Mitochondrial function is crucial for cancer cell survival and metastasis.
- BCS1L generates two isoforms: full-length BCS1L-L and short BCS1L-S.
- BCS1L-L is elevated in cancers and boosts oxidative phosphorylation and ATP production.
- BCS1L-S fails to localize to mitochondria, impairing metabolic function.
- Splicing factor USP39 promotes exon 2 inclusion, generating oncogenic BCS1L-L.
- Splice-switch ASOs induce exon 2 skipping, reducing BCS1L-L and tumor growth.
- Targeting BCS1L-L with ASOs is a novel approach for ovarian cancer treatment.