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  3. Aberrant Nuclear Localization Of Ebp50 Promotes Colorectal Carcinogenesis In Xenotransplanted Mice By Modulating Tcf-1 And Β-catenin Interactions.
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  3. Aberrant Nuclear Localization Of Ebp50 Promotes Colorectal Carcinogenesis In Xenotransplanted Mice By Modulating Tcf-1 And Β-catenin Interactions.

Related Experiment Video

In vitro Organoid Culture of Primary Mouse Colon Tumors
07:33

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Published on: May 17, 2013

Aberrant nuclear localization of EBP50 promotes colorectal carcinogenesis in xenotransplanted mice by modulating

Yu-Yu Lin1, Yung-Ho Hsu, Hsin-Yi Huang

  • 1Graduate Institute of Molecular Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.

The Journal of Clinical Investigation
|April 3, 2012

View abstract on PubMed

Summary
This summary is machine-generated.

ERM-binding phosphoprotein 50 (EBP50) in the nucleus promotes colon cancer by stabilizing beta-catenin interactions with TCF-1. Reducing EBP50 inhibits tumor growth and cell cycle progression.

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Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Canonical Wnt signaling dysregulation is implicated in colon carcinogenesis.
  • Beta-catenin is a key mediator, transactivating gene expression upon Wnt activation.
  • The balance between TCF-1 forms is crucial but not fully understood.

Purpose of the Study:

  • To investigate the role of ERM-binding phosphoprotein 50 (EBP50) in colon carcinogenesis.
  • To elucidate EBP50's mechanism in modulating beta-catenin and TCF-1 interactions.
  • To determine the impact of EBP50 on Wnt/beta-catenin signaling and tumor progression.

Main Methods:

  • Analysis of EBP50 localization in colorectal cancer cell lines and tumors.
  • Assessment of EBP50's effect on beta-catenin/TCF-1 complex formation.
  • Genome-wide occupancy analysis and chromatin immunoprecipitation assays.
  • EBP50 knockdown experiments in cell lines and in vivo tumorigenesis models.

    • Main Results:

    • Nuclear EBP50 was observed in aggressive colorectal tumors and cell lines at low densities.
    • EBP50 stabilized beta-catenin/TCF-1 complexes and formed a ternary complex with dnTCF-1.
    • This complex enhanced Wnt/beta-catenin signaling, increasing oncogene transcription (c-Myc, cyclin D1).
    • EBP50 binds to genomic regions with TCF/LEF motifs.
    • EBP50 knockdown reduced cell cycle progression, anchorage-independent growth, and tumorigenesis.

    Conclusions:

    • Nuclear EBP50 facilitates colon tumorigenesis by modulating beta-catenin and TCF-1 interactions.
    • EBP50 acts as a crucial facilitator of Wnt/beta-catenin signaling in colorectal cancer.
    • Targeting EBP50 may offer a therapeutic strategy for colon cancer.