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WDR5 high expression and its effect on tumorigenesis in leukemia
Zheng Ge1,2,3, Evelyn J Song2, Yuka Imamura Kawasawa4
1Department of Hematology (Key Department of Jiangsu Medicine), Zhongda Hospital, Southeast University Medical School, Nanjing, Jiangsu, China.
Oncotarget
|May 19, 2016
Summary
WD repeat domain 5 (WDR5) is elevated in leukemia, correlating with high-risk disease and poor remission. WDR5 knockdown inhibits cancer cell growth by affecting gene transcription and H3K4 methylation, suggesting an oncogenic role.
Area of Science:
- Epigenetics
- Molecular Biology
- Oncology
Background:
- WD repeat domain 5 (WDR5) is crucial for epigenetic gene regulation.
- The specific role of WDR5 in leukemia pathogenesis is not well understood.
Purpose of the Study:
- To investigate the oncogenic role of WDR5 in leukemia.
- To explore the mechanism of WDR5 in regulating gene transcription and its association with H3K4 methylation in leukemic cells.
Main Methods:
- Analysis of WDR5 expression in leukemia patients.
- Genome-wide WDR5 binding site identification.
- WDR5 knockdown using shRNA.
- Assessment of cell proliferation, apoptosis, and target gene expression.
- Chromatin immunoprecipitation for H3K4me3 enrichment.
Main Results:
- WDR5 expression is upregulated in leukemia patients and associated with high-risk disease.
- High WDR5 and MLL1 expression correlates with a lower complete remission rate.
- WDR5 binds globally in leukemic cells, co-localizing with H3K4me3.
- WDR5 knockdown reduces proliferation, induces apoptosis, and decreases target gene expression and H3K4me3 enrichment.
Conclusions:
- WDR5 exhibits an oncogenic effect in leukemia.
- WDR5-mediated H3K4 methylation is a key mechanism in leukemogenesis.
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