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SRSF1 Prevents DNA Damage and Promotes Tumorigenesis through Regulation of DBF4B Pre-mRNA Splicing

Linlin Chen1, Chunling Luo1, Lei Shen2

  • 1Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.

Cell Reports
|December 21, 2017
PubMed

Insights

The splicing factor SRSF1 promotes DBF4B exon6 inclusion, crucial for colon cancer cell proliferation and genomic stability. SRSF1 and DBF4B-FL are potential prognostic factors in colorectal cancer.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Alternative splicing dysregulation is linked to cancer, but mechanisms are unclear.
  • The splicing factor SRSF1's role in cancer is under investigation.

Purpose of the Study:

  • To investigate the role of SRSF1 in regulating DBF4B splicing in colon cancer.
  • To determine the functional significance of the DBF4B exon6-containing isoform (DBF4B-FL) in tumorigenesis.

Main Methods:

  • Investigated SRSF1 binding and regulation of DBF4B exon6 splicing.
  • Utilized in vitro and in vivo models (colon cancer cells, mice) to assess the impact of DBF4B-FL and SRSF1.
  • Analyzed clinical colorectal cancer samples for SRSF1 and DBF4B exon6 inclusion levels.

Main Results:

  • SRSF1 specifically promotes DBF4B exon6 inclusion.
  • DBF4B-FL and SRSF1 are essential for colon cancer cell proliferation and genomic stability.
  • SRSF1 inactivation mimics DBF4B-FL depletion effects.
  • DBF4B-FL overexpression rescues growth defects and DNA damage from SRSF1 knockdown.
  • Increased DBF4B exon6 inclusion correlates with SRSF1 upregulation in clinical colorectal cancer.

Conclusions:

  • SRSF1 is a key regulator of DBF4B pre-mRNA splicing in colon cancer.
  • SRSF1-mediated DBF4B exon6 splicing is critical for colon cancer progression.
  • SRSF1 and DBF4B-FL represent potential prognostic biomarkers for colorectal cancer.

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