Related Experiment Video
Updated: Jul 31, 2025

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
Published on: June 27, 2020
Forkhead box protein D2 suppresses colorectal cancer by reprogramming enhancer interactions
Hyo-Min Kim1, Byunghee Kang1, Sohyun Park1
1Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 37673, Republic of Korea.
Forkhead box protein D2 (FOXD2) suppresses colorectal cancer by regulating gene expression in intestinal stem cells. Overexpression of FOXD2 rewires chromatin interactions, promoting apoptosis and potentially offering a new therapeutic target.
Area of Science:
- Cell Biology
- Molecular Biology
- Oncology
Background:
- Somatic stem cells maintain tissue homeostasis, with epigenomic regulation crucial for identity and disease.
- Enhancers control gene expression spatially and temporally, and their dysregulation contributes to tumorigenesis.
Purpose of the Study:
- To investigate the role of forkhead box protein D2 (FOXD2) in the gene regulatory network of large intestinal stem cells.
- To elucidate the mechanism by which FOXD2 influences colorectal cancer development and regression.
Main Methods:
- Epigenomic and transcriptomic analyses were employed.
- Investigated FOXD2's interaction with chromatin and its effect on gene regulation.
- Assessed the impact of FOXD2 on p53-responsive genes and apoptosis induction.
Main Results:
- FOXD2 acts as a hub in the gene regulatory network specific to large intestinal stem cells.
- FOXD2 overexpression promotes colon cancer regression by facilitating MLL4/KMT2D binding and H3K4 monomethylation.
- FOXD2-mediated chromatin interactions alter the regulation of p53-responsive genes, leading to apoptosis.
Conclusions:
- FOXD2 plays a novel role in suppressing colorectal cancer growth through chromatin modulation.
- FOXD2 functions as a chromatin-tuning factor with potential as a therapeutic target for colorectal cancer.
Related Concept Videos
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Co-activators and Co-repressors
Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Abnormal Proliferation
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...

