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Updated: Feb 14, 2026
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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
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Splicing Factor 3a Subunit 1 Promotes Colorectal Cancer Growth via Anti-Apoptotic Effects of Syntaxin12.
Takahiro Sasaki1, Hiroaki Konishi2, Tatsuya Dokoshi3
1Division of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
International Journal of Molecular Sciences
|February 13, 2026
Summary
Splicing factor 3A1 (SF3A1) promotes colorectal cancer (CRC) growth by preventing cancer cell death. Targeting the SF3A1-Syntaxin 12 (STX12) pathway offers a selective therapeutic strategy for CRC.
Area of Science:
- Molecular Biology
- Cancer Research
- RNA Biology
Background:
- Aberrant RNA-binding proteins (RBPs) are implicated in cancer development.
- The specific roles of individual RBPs in tumorigenesis require further elucidation.
Purpose of the Study:
- To investigate the role of Splicing factor 3A1 (SF3A1) in colorectal cancer (CRC) progression.
- To identify downstream targets and mechanisms through which SF3A1 influences CRC cell viability and apoptosis.
Main Methods:
- Cell proliferation and apoptosis assays (TUNEL, PARP, caspase-3/7) in CRC and non-cancerous cells.
- Xenograft mouse model studies to assess SF3A1's in vivo tumor-promoting function.
- Transcriptome analysis and RNA-immunoprecipitation (RIP) to identify SF3A1 targets.
Main Results:
- SF3A1 downregulation suppressed CRC cell proliferation with minimal impact on normal cells.
- SF3A1 was found to inhibit apoptosis in CRC cells.
- Syntaxin 12 (STX12) was identified as a downstream effector, stabilized by SF3A1.
- STX12 knockdown induced apoptosis in CRC cells, confirming its role in SF3A1-mediated resistance.
Conclusions:
- SF3A1 promotes CRC progression by stabilizing STX12 mRNA, thereby conferring apoptosis resistance.
- The SF3A1-STX12 regulatory axis represents a novel and selective therapeutic target for colorectal cancer.
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