Fig. 8
From: SF3B3-regulated mTOR alternative splicing promotes colorectal cancer progression and metastasis
Mechanistic model illustrating the role of SF3B3 in CRC. SF3B3 is upregulated in CRC tissues, promoting CRC tumorigenesis and metastasis. Targeting SF3B3 through RNA silencing downregulates mTORα via alternative splicing, resulting in the induction of autophagy, suppression of SREBF1 transcription, and inhibition of SREBF1 protein activation. Consequently, silencing of SF3B3 prevents CRC progression and metastasis by inhibiting lipogenesis and promoting apoptosis