| Literature DB >> 33397955 |
Hu Lei1, Han-Zhang Xu1, Hui-Zhuang Shan1, Meng Liu1, Ying Lu1, Zhi-Xiao Fang1, Jin Jin1, Bo Jing1, Xin-Hua Xiao1, Shen-Meng Gao2, Feng-Hou Gao3, Li Xia1, Li Yang1, Li-Gen Liu1, Wei-Wei Wang1, Chuan-Xu Liu4, Yin Tong5, Yun-Zhao Wu1, Jun-Ke Zheng1, Guo-Qiang Chen6, Li Zhou7, Ying-Li Wu8.
Abstract
Identifying novel drug targets to overcome resistance to tyrosine kinase inhibitors (TKIs) and eradicating leukemia stem/progenitor cells are required for the treatment of chronic myelogenous leukemia (CML). Here, we show that ubiquitin-specific peptidase 47 (USP47) is a potential target to overcome TKI resistance. Functional analysis shows that USP47 knockdown represses proliferation of CML cells sensitive or resistant to imatinib in vitro and in vivo. The knockout of Usp47 significantly inhibits BCR-ABL and BCR-ABLT315I-induced CML in mice with the reduction of Lin-Sca1+c-Kit+ CML stem/progenitor cells. Mechanistic studies show that stabilizing Y-box binding protein 1 contributes to USP47-mediated DNA damage repair in CML cells. Inhibiting USP47 by P22077 exerts cytotoxicity to CML cells with or without TKI resistance in vitro and in vivo. Moreover, P22077 eliminates leukemia stem/progenitor cells in CML mice. Together, targeting USP47 is a promising strategy to overcome TKI resistance and eradicate leukemia stem/progenitor cells in CML.Entities:
Year: 2021 PMID: 33397955 DOI: 10.1038/s41467-020-20259-0
Source DB: PubMed Journal: Nat Commun ISSN: 2041-1723 Impact factor: 14.919