Antitumor Effects of Blocking Protein Neddylation in T315I-BCR-ABL Leukemia Cells and Leukemia Stem Cells

Imatinib revolutionized the treatment of chronic myeloid leukemia (CML), but drug resistance and disease recurrence remain a challenge. In this study, we suggest a novel strategy based on blocking protein neddylation to address BCR-ABL point mutations and leukemia stem cells (LSC) that lie at the ro...

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Veröffentlicht in:	Cancer research (Chicago, Ill.) Ill.), 2018-03, Vol.78 (6), p.1522-1536
Hauptverfasser:	Liu, Chang, Nie, Danian, Li, Juan, Du, Xin, Lu, Yuhong, Li, Yangqiu, Zhou, Jingfeng, Jin, Yanli, Pan, Jingxuan
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antigens, CD34 - metabolism Antineoplastic Agents - pharmacology Antitumor activity Apoptosis Apoptosis - drug effects Apoptosis - genetics BCR-ABL protein Cancer CD34 antigen Cell Line, Tumor Cell self-renewal Chronic myeloid leukemia Cyclin-dependent kinase inhibitor p27 Cyclopentanes - pharmacology Disease resistance Drug resistance Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics Fusion protein Fusion Proteins, bcr-abl - genetics Humans Imatinib Imatinib Mesylate - pharmacology Leukemia Leukemia, Experimental - drug therapy Leukemia, Experimental - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Male Mice Mice, Inbred C57BL Molecular Targeted Therapy - methods Mutation Myeloid leukemia Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - pathology Nuclei p53 Protein Point Mutation Protein turnover Proteins Pyrimidines - pharmacology Stem cell transplantation Stem cells Therapeutic applications Ubiquitin-Activating Enzymes - antagonists & inhibitors Ubiquitin-Activating Enzymes - metabolism
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