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Related Experiment Video

Updated: May 23, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors

In vitro Organoid Culture of Primary Mouse Colon Tumors

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

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.