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Updated: Sep 15, 2025

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells
Published on: June 30, 2023
Splicing factor 3b subunit 4 (SF3b4) is mediated by EP300 and CREBBP to promote colorectal cancer (CRC) proliferation
Tianhao Wu1, Zhongxiang Xiao1, Bowen Su1
1Department of Gastrointestinal Surgery, Affiliated Hospital of North Sichuan Medical College/Institute of Hepatobiliary Pancreatic and Intestinal Disease, North Sichuan Medical College Nanchong, Sichuan, China.
Abstract:
Splicing factor 3b subunit 4 (SF3b4) is closely associated with cancer development. As a core subunit of the SF3b complex, SF3b4 participates in regulating alternative splicing, and its abnormal expression is linked to the onset of malignant tumors. However, the role of SF3b4 in colorectal cancer (CRC) remains undefined. This study demonstrates that in CRC, E1A binding protein p300 (EP300) and CREB binding protein (CREBBP) regulate SF3b4 expression by activating Histone H3 lysine 27 acetylation (H3K27ac) on the SF3b4 promoter. Additionally, enhanced autophagy counteracts the proliferation-inhibitory effect of SF3b4 knockdown in CRC cells. Implications Statement: SF3b4 may promote CRC proliferation by enhancing cellular autophagy. SF3b4 acts as a potential oncogene in CRC tumorigenesis and progression. SF3b4 serves as a promising prognostic biomarker for CRC.
Insights
Splicing factor 3b subunit 4 (SF3b4) promotes colorectal cancer (CRC) by enhancing autophagy. This potential oncogene may serve as a prognostic biomarker for CRC patients.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Splicing factor 3b subunit 4 (SF3b4) is implicated in cancer development due to its role in alternative splicing.
- Abnormal SF3b4 expression is linked to malignant tumor onset, but its specific function in colorectal cancer (CRC) is unclear.
Purpose of the Study:
- To elucidate the role of SF3b4 in colorectal cancer (CRC) pathogenesis.
- To investigate the regulatory mechanisms of SF3b4 expression and its functional impact on CRC cells.
Main Methods:
- Analysis of SF3b4 expression in CRC.
- Investigation of epigenetic regulation by EP300 and CREBBP via H3K27ac on the SF3b4 promoter.
- Assessment of SF3b4 knockdown effects on CRC cell proliferation and autophagy.
Main Results:
- EP300 and CREBBP regulate SF3b4 expression in CRC through H3K27ac activation on the SF3b4 promoter.
- SF3b4 knockdown inhibits CRC cell proliferation, an effect counteracted by enhanced autophagy.
- SF3b4 appears to promote CRC proliferation by upregulating cellular autophagy.
Conclusions:
- SF3b4 functions as a potential oncogene in colorectal cancer tumorigenesis and progression.
- SF3b4 may promote CRC proliferation by enhancing cellular autophagy.
- SF3b4 presents as a promising prognostic biomarker for CRC.
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