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  11. Fev-mediated Wnt2 Transcription Is Involved In The Progression Of Colorectal Cancer Via The Wnt Signaling

FEV-mediated WNT2 transcription is involved in the progression of colorectal cancer via the Wnt signaling

Xia Zhang1, Lingshu Yang1, Jianing Liu1

  • 1Department of General Surgery, The Fourth Affiliated Hospital of Harbin Medical University, No. 37, Yiyuan Street, Nangang District, Harbin, 150001 Heilongjiang China.

Cytotechnology
|October 22, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

The transcription factor fifth Ewing variant protein (FEV) is downregulated in colorectal cancer (CRC). Restoring FEV inhibits CRC growth by repressing WNT2, revealing a novel FEV/WNT2 axis critical for cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer mortality globally.
  • The molecular mechanisms driving CRC progression require further elucidation.
  • Transcription factors play crucial roles in cancer development.

Purpose of the Study:

  • To investigate the role of the transcription factor fifth Ewing variant protein (FEV) in colorectal cancer.
  • To uncover the underlying molecular mechanism of FEV in CRC.
  • To identify potential therapeutic targets within the FEV signaling pathway.

Main Methods:

  • Analysis of transcriptome differential expression in human CRC and adjacent tissues using public datasets (GSE143939, GSE142279, GSE196006, GSE200427).
  • Screening of intersecting genes against the Human TFBD database for transcription factors.
Keywords:
Colorectal cancerFEVWNT2Wnt signaling pathway

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  • KEGG enrichment analysis to identify enriched pathways.
  • Investigation of FEV binding to the WNT2 promoter and its effect on WNT2 transcription.

    • Main Results:

    • FEV expression was significantly reduced in CRC tissues.
    • Upregulation of FEV inhibited CRC cell growth and tumor progression.
    • The Wnt signaling pathway, initiated by WNT2, was highly enriched in CRC.
    • FEV directly repressed WNT2 transcription by binding to its promoter.
    • WNT2 promoted CRC cell proliferation, migration, and invasion.

    Conclusions:

    • A novel FEV/WNT2 signaling axis is identified as critical for colorectal cancer progression.
    • FEV acts as a tumor suppressor in CRC by inhibiting WNT2.
    • Targeting the FEV/WNT2 axis presents a potential therapeutic strategy for CRC patients.
    β-catenin