| Literature DB >> 28401191 |
Stefanie Göllner1, Carsten Müller-Tidow1.
Abstract
The polycomb protein enhancer of zeste homolog 2 (EZH2) may have a dual role in cancer pathogenesis acting as an oncogene or as a tumor suppressor depending on the cancer type. We recently demonstrated that proteasomal degradation of EZH2 resulting from cyclin-dependent kinase 1 (CDK1)-induced phosphorylation at Threonine (T) 487 represents a novel mechanism of drug resistance in acute myeloid leukemia (AML). Our findings suggest that restoration of EZH2 protein is a viable approach to overcome therapy resistance in AML.Entities:
Keywords: Acute myeloid leukemia (AML); EZH2; drug resistance; epigenetic; proteasome
Year: 2017 PMID: 28401191 PMCID: PMC5383362 DOI: 10.1080/23723556.2017.1291396
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556