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The EMT modulator SNAI1 contributes to AML pathogenesis via its interaction with LSD1
Catherine L Carmichael1, Jueqiong Wang1, Thao Nguyen1
1Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, Australia.
Blood
|May 6, 2020
Summary
Overexpression of SNAI1, an epithelial-to-mesenchymal transition (EMT) modulator, drives acute myeloid leukemia (AML) by impairing cell differentiation and promoting proliferation. This occurs through interaction with histone demethylase KDM1A/LSD1.
Area of Science:
- Hematology
- Cancer Biology
- Molecular Oncology
Background:
- Epithelial-to-mesenchymal transition (EMT) modulators are increasingly recognized in leukemia.
- The precise role of EMT modulators in leukemia pathogenesis requires further investigation.
Purpose of the Study:
- To elucidate the role of SNAI1, a key EMT modulator, in acute myeloid leukemia (AML).
- To investigate the underlying mechanisms by which SNAI1 contributes to AML development.
Main Methods:
- Analysis of SNAI1 expression in human AML.
- Ectopic expression of Snai1 in mouse hematopoietic cells.
- Investigation of the interaction between SNAI1 and KDM1A/LSD1.
Main Results:
- SNAI1 overexpression is pathologically relevant in human AML.
- SNAI1 contributes to impaired differentiation, enhanced self-renewal, and proliferation of myeloid cells.
- Ectopic Snai1 expression in hematopoietic cells predisposes mice to AML via interaction with KDM1A/LSD1.
Conclusions:
- SNAI1 plays a significant role in leukemia development.
- SNAI1 contributes to AML pathogenesis through interaction with KDM1A/LSD1, representing a novel mechanism of LSD1 corruption in cancer.
- These findings are relevant to the therapeutic targeting of LSD1 inhibitors in AML and other malignancies.
