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GLIS2 promotes colorectal cancer through repressing enhancer activation
Jie Yao1, Pin-Ji Lei1, Qing-Lan Li1
1Frontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Wuhan University, Wuhan, Hubei, 430072, China.
Oncogenesis
|June 3, 2020
Summary
Researchers identified new regulators for p53 transcription, finding GLIS2 promotes apoptosis and cell migration. GLIS2 acts as an oncogene by repressing enhancer activation in colon cancer.
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- Gene transcription is controlled by multiple transcription factors.
- A systematic method to identify transcription factor co-regulators is needed.
Purpose of the Study:
- To identify co-regulators for p53-mediated transcription.
- To investigate the role of GLIS2 in p53 target gene regulation and cancer.
Main Methods:
- Chromatin immunoprecipitation sequencing (ChIP-Seq) was performed.
- Computational analysis predicted transcription factor regulators.
- Functional assays validated the roles of GLIS2, MAZ, and MEF2A.
Main Results:
- GLIS2, MAZ, and MEF2A were confirmed as regulators of p53 target genes.
- GLIS2 selectively regulates PUMA, not p21, increasing apoptosis.
- GLIS2 represses enhancer H3K27ac, inhibits p300, and promotes cell migration.
Conclusions:
- Candidate p53 transcriptional regulators were predicted.
- GLIS2 functions as an oncogene in colon cancer by inhibiting enhancer activation.
- GLIS2 plays a role in regulating apoptosis, cell migration, and focal adhesion gene expression.
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