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Home
Research Domains
Biomedical And Clinical Sciences
Oncology And Carcinogenesis
Predictive And Prognostic Markers
Bmi1 And Mel18 Promote Colitis-associated Cancer In Mice Via Reg3b And Stat3.

Home
Research Domains
Biomedical And Clinical Sciences
Oncology And Carcinogenesis
Predictive And Prognostic Markers
Bmi1 And Mel18 Promote Colitis-associated Cancer In Mice Via Reg3b And Stat3.

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BMI1 and MEL18 Promote Colitis-Associated Cancer in Mice via REG3B and STAT3.

Xicheng Liu¹, Wendi Wei¹, Xiaowei Li²

¹National Institute of Biological Sciences, Beijing, China.

Gastroenterology

|August 7, 2017

View abstract on PubMed

Summary

This summary is machine-generated.

Disrupting BMI1 and MEL18 in mice reduced colitis-associated cancer by suppressing proliferation and increasing apoptosis. This suggests targeting the Reg3b-STAT3 pathway may prevent cancer in patients with colitis.

Keywords:

Colon Cancer PAP PcG Ulcerative Colitis

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Published on: April 21, 2015

Area of Science:

Epigenetics
Cancer Biology
Gastroenterology

Background:

Polycomb group proteins, including BMI1 and MEL18, are epigenetic factors involved in gene silencing.
Dysregulation of these proteins is observed in cancer cells, but their role in colitis-associated cancer (CAC) is unclear.

Purpose of the Study:

To investigate the involvement of BMI1 and MEL18 in the initiation and progression of CAC in mice.
To elucidate the underlying molecular mechanisms, including the role of Reg3b and STAT3 signaling.

Main Methods:

Generated mice with conditional disruption of Bmi1 and Mel18 specifically in intestinal epithelial cells (IECs).
Induced CAC using azoxymethane (AOM) and dextran sulfate sodium (DSS) treatment.
Analyzed colon tissues via histology and immunoblotting; performed cDNA microarray analyses on isolated IECs.

Main Results:

Mice with combined Bmi1 and Mel18 disruption (DKO mice) developed significantly fewer and less severe polyps compared to controls.
DKO mice exhibited reduced proliferation, increased apoptosis, and elevated Reg3b expression in colon tissues.
Reg3b suppressed cytokine-induced STAT3 activation in IECs, and human REG3B expression correlated inversely with pSTAT3 and patient survival.

Conclusions:

BMI1 and MEL18 promote CAC development by suppressing Reg3b expression, thereby enhancing proliferation and reducing apoptosis.
Reg3b negatively regulates STAT3 activation in colon epithelial cells.
Targeting the BMI1/MEL18-Reg3b-STAT3 pathway presents a potential therapeutic strategy for preventing CAC in patients with colitis.