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.

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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