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Updated: Apr 3, 2026
06:01
A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
Published on: July 6, 2017
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Prostaglandin E receptor 4 (EP4) promotes colonic tumorigenesis
Jian Chang1,2,3, Jean Vacher4, Bing Yao1
1Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.
Oncotarget
|September 18, 2015
Summary
Targeting the EP4 receptor in myeloid cells significantly reduced colorectal cancer (CRC) growth in mice. This finding suggests EP4 as a promising target for CRC prevention and treatment.
Area of Science:
- Oncology
- Immunology
- Gastroenterology
Background:
- Colorectal cancer (CRC) is a significant health burden.
- Tumor-host interactions, particularly with myeloid cells, influence CRC progression.
- Prostaglandins, especially PGE2, play a key role in CRC development.
Purpose of the Study:
- To investigate the role of the PGE2 receptor subtype EP4 in myeloid cells in CRC development.
- To determine if targeting myeloid cell EP4 can inhibit tumor formation.
Main Methods:
- Selective ablation of EP4 in myeloid cells of ApcMin/+ mice (a model for intestinal adenomatous polyposis).
- Analysis of adenoma formation, size, and associated molecular signaling (mTOR, ERK).
- Assessment of macrophage/dendritic cell phenotype following EP4 inhibition.
Main Results:
- Myeloid cell-specific EP4 deletion markedly inhibited adenoma number and size in ApcMin/+ mice.
- Inhibition of EP4 signaling decreased mTOR and ERK activation.
- Genetic or pharmacologic EP4 inhibition induced an anti-tumorigenic M1 phenotype in myeloid cells.
Conclusions:
- PGE2-mediated EP4 signaling in myeloid cells promotes colorectal cancer tumorigenesis.
- EP4 is a potential therapeutic target for CRC chemoprevention and treatment.
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