The abstract is read at the publisher; the summary is JClub's.
Trunc-APC, produced by truncating APC in colorectal cancer cells, binds pre-mRNA through its N-terminal 1–169 region to broadly regulate alternative splicing.
- Why it matters: Truncating APC is a key CRC driver, but the post-transcriptional and oncogenic functions of the resulting truncated protein were unclear.
- What they did: In CRC cells, Trunc-APC promotes exon inclusion in ARHGEF11 and interacts with DDX21 to facilitate SF3B complex recruitment to pre-mRNA; Madrasin was tested in ApcMin/+ mice.
- The result: Trunc-APC–driven splicing is linked to increased Bcl-xL/BAX complex formation and reduced apoptosis, and Madrasin significantly reduced tumor burden in ApcMin/+ CRC mice, supporting targeting the Trunc-APC/DDX21/SF3B axis.
The findingWhy it mattersWhat they didThe result
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