Journal
CANCER CELL
Volume 18, Issue 6, Pages 606-618Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2010.10.032
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Funding
- CRUK
- AICR
- Kay Kendall Leukaemia Fund
- [037632]
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Identification of molecular pathways essential for cancer stem cells is critical for understanding the underlying biology and designing effective cancer therapeutics. Here, we demonstrated that beta-catenin was activated during development of MLL leukemic stem cells (LSCs). Suppression of beta-catenin reversed LSCs to a pre-LSC-like stage and significantly reduced the growth of human MLL leukemic cells. Conditional deletion of beta-catenin completely abolished the oncogenic potential of MLL-transformed cells. In addition, established MLL LSCs that have acquired resistance against GSK3 inhibitors could be resensitized by suppression of beta-catenin expression. These results unveil previously unrecognized multifaceted functions of beta-catenin in the establishment and drug-resistant properties of MLL stem cells, highlighting it as a potential therapeutic target for an important subset of AMLs.
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