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Serine/arginine-rich splicing factor 7 regulates p21-dependent growth arrest in colon cancer cells

Saki Saijo1, Yuki Kuwano, Kiyoshi Masuda

  • 1Department of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School.

The Journal of Medical Investigation : JMI
|September 21, 2016
PubMed

Insights

SRSF7 knockdown inhibits colon cancer cell growth by affecting cell cycle regulators. This study reveals SRSF7

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • Serine/arginine-rich splicing factors (SRSFs) are crucial for gene expression and pre-mRNA splicing.
  • SRSF7 is implicated in various cellular processes, including cancer development.

Purpose of the Study:

  • To investigate the role of SRSF7 in colon cancer cell proliferation.
  • To elucidate the molecular mechanisms underlying SRSF7's function in colon cancer.

Main Methods:

  • SRSF7 knockdown in HCT116 colon cancer cells.
  • Gene expression analysis (4,499 genes altered).
  • Ingenuity Pathway Analysis (IPA) for pathway enrichment.
  • Western blotting to assess protein levels (p21, p53, CDK2, Rb).
  • Analysis of CDKN1A mRNA stability and promoter activity.

Main Results:

  • SRSF7 knockdown inhibited HCT116 cell growth.
  • Cell cycle regulation pathways were significantly enriched.
  • p21 levels increased post-transcriptionally, independent of p53.
  • CDKN1A mRNA stabilized, and p21 degradation was blocked.
  • Cell growth inhibition occurred in p53-null cells, indicating p53-independent mechanisms.

Conclusions:

  • SRSF7 plays a significant role in colon cancer cell proliferation.
  • SRSF7 regulates p21 levels through post-transcriptional mechanisms, including mRNA stabilization and blocking protein degradation.
  • These findings highlight SRSF7 as a potential therapeutic target in colon cancer.

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