Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10909103 | Leukemia Research | 2013 | 8 Pages |
Abstract
Chronic myeloid leukemia (CML) is associated with overexpression of BCR-ABL1, a nonreceptor tyrosine kinase critical for malignant transformation. We investigated whether non-coding microRNAs (miRNAs) targeting BCR-ABL1 mRNA contribute to the pathogenesis of CML. Indeed, miR-30a targeted BCR-ABL1 and was underexpressed in bone marrow from CML patients. In K562 leukemia cells, overexpression of miR-30a reduced ABL1 and BCR-ABL1 protein expression, decreased proliferation, and arrested cell cycle progression between G1 and S. These findings strongly suggest that miR-30a acts as a tumor suppressor by downregulating ABL1 and BCR-ABL1 expression. Upregulation of miR-30a in hematopoietic cells may have therapeutic efficacy against CML.
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Authors
Yue Liu, Yanbin Song, Wenli Ma, Wenling Zheng, Hong Yin,