Correction: MPT0B169, a New Antitubulin Agent, Inhibits Bcr-Abl Expression and Induces Mitochondrion-Mediated Apoptosis in Nonresistant and Imatinib-Resistant Chronic Myeloid Leukemia Cells
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{"title"=>"Correction: MPT0B169, a new antitubulin agent, inhibits Bcr-Abl expression and induces mitochondrion-mediated apoptosis in nonresistant and imatinib-resistant chronic myeloid leukemia cells (PLoS ONE (2016) 11:1 (e0148093) DOI: 10.1371/journal.pone.0148093)", "type"=>"generic", "authors"=>[{"first_name"=>"Shuit Mun", "last_name"=>"Wong", "scopus_author_id"=>"57116918100"}, {"first_name"=>"Fu Hwa", "last_name"=>"Liu", "scopus_author_id"=>"36062982500"}, {"first_name"=>"Yueh Lun", "last_name"=>"Lee", "scopus_author_id"=>"8747699800"}, {"first_name"=>"Huei Mei", "last_name"=>"Huang", "scopus_author_id"=>"8591040600"}], "year"=>2017, "source"=>"PLoS ONE", "identifiers"=>{"pui"=>"618698348", "doi"=>"10.1371/journal.pone.0186531", "issn"=>"19326203", "pmid"=>"26815740", "sgr"=>"85030979610", "scopus"=>"2-s2.0-85030979610"}, "id"=>"12fc92dc-d1d7-31f3-9a1c-f2bc581f7298", "abstract"=>"Chronic myeloid leukemia (CML) is a clonal disorder of hematopoietic stem/progenitor cells that is caused by the Bcr-Abl oncoprotein. Clinical resistance to the Bcr-Abl inhibitor imatinib is a critical problem in treating CML. This study investigated the antitumor effect and mechanism of MPT0B169, a new antitubulin agent, in K562 CML cells and their derived imatinib-resistant cells, IMR2 and IMR3. IMR2 and IMR3 cells showed complete resistance to imatinib-induced growth inhibition and apoptosis. Resistance involved ERK1/2 overactivation and MDR1 overexpression. MPT0B169 inhibited the growth of K562, IMR2, and IMR3 cells in a dose- and time-dependent manner. MPT0B169 substantially inhibited the mRNA and protein levels of Bcr-Abl, followed by its downstream pathways including Akt, ERK1/2, and STAT3 in these cells. MPT0B169 treatment resulted in a decrease in the polymer form of tubulin according to Western blot analysis. It triggered cell cycle arrest at the G2/M phase before apoptosis, which was related to the upregulation of the mitotic marker MPM2 and the cyclin B1 level, and a change in the phosphorylation of Cdk1. MPT0B169 induced apoptosis in nonresistant and imatinib-resistant cells via a mitochondrion-mediated caspase pathway. Further study showed that the agent led to a decrease in the antiapoptotic proteins Bcl-2, Bcl-xL, and Mcl-1 and an increase in the apoptotic protein Bax. Taken together, our results suggest that MPT0B169 might be a promising agent for overcoming imatinib resistance in CML cells.", "link"=>"http://www.mendeley.com/research/correction-mpt0b169-new-antitubulin-agent-inhibits-bcrabl-expression-induces-mitochondrionmediated-a", "reader_count"=>5, "reader_count_by_academic_status"=>{"Librarian"=>1, "Researcher"=>1, "Student > Ph. D. Student"=>1, "Student > Master"=>2}, "reader_count_by_user_role"=>{"Librarian"=>1, "Researcher"=>1, "Student > Ph. D. Student"=>1, "Student > Master"=>2}, "reader_count_by_subject_area"=>{"Agricultural and Biological Sciences"=>2, "Medicine and Dentistry"=>1, "Chemistry"=>1, "Computer Science"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>1}, "Chemistry"=>{"Chemistry"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>2}, "Computer Science"=>{"Computer Science"=>1}}, "group_count"=>0}

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