Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant. [electronic resource]
Producer: 20190617Description: 68 p. digitalISSN:- 2041-4889
- Animals
- Anthelmintics -- pharmacology
- Apoptosis -- drug effects
- Cell Proliferation -- drug effects
- Down-Regulation -- drug effects
- Drug Resistance, Neoplasm -- drug effects
- Fusion Proteins, bcr-abl -- genetics
- Imatinib Mesylate -- pharmacology
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive -- genetics
- Mice, Nude
- Mitochondria -- drug effects
- Mitogen-Activated Protein Kinase Kinases -- antagonists & inhibitors
- Models, Biological
- Mutation -- genetics
- Myeloid Cell Leukemia Sequence 1 Protein -- metabolism
- Niclosamide -- pharmacology
- Protein Kinase Inhibitors -- pharmacology
- Signal Transduction -- drug effects
- Sp1 Transcription Factor -- metabolism
- Survival Analysis
- Transcription, Genetic -- drug effects
- X-Linked Inhibitor of Apoptosis Protein -- metabolism
- Xenograft Model Antitumor Assays
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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