ArticleCancer research2007
MUC1 oncoprotein regulates Bcr-Abl stability and pathogenesis in chronic myelogenous leukemia cells.
Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Integrating Clinical Cancer and PTM Proteomics Data Identifies a Mechanism of ACK1 Kinase Activation.Molecular cancer research : MCR · 2024Article
- Regulatory Molecules and Corresponding Processes of BCR-ABL Protein Degradation.Journal of Cancer · 2019Review
- CD69 partially inhibits apoptosis and erythroid differentiation via CD24, and their knockdown increase imatinib sensitivity in BCR-ABL-positive cells.Journal of cellular physiology · 2018Article
- Novel Antigen Targets for Immunotherapy of Acute Myeloid Leukemia.Current drug targets · 2017Review
- MUC1 in hematological malignancies.Leukemia & lymphoma · 2016Review
- Enhancing potency of siRNA targeting fusion genes by optimization outside of target sequence.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The generation and analyses of a novel combination of recombinant adenovirus vaccines targeting three tumor antigens as an immunotherapeutic.Oncotarget · 2015Article
- Stat5 Exerts Distinct, Vital Functions in the Cytoplasm and Nucleus of Bcr-Abl+ K562 and Jak2(V617F)+ HEL Leukemia Cells.Cancers · 2015Article
- The adenocarcinoma cell surface mucin receptor for alpha-fetoprotein: is the same receptor present on circulating monocytes and macrophages? A commentary.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- Protein mislocalization: mechanisms, functions and clinical applications in cancer.Biochimica et biophysica acta · 2014Review
- Identification and characterization of agonist epitopes of the MUC1-C oncoprotein.Cancer immunology, immunotherapy : CII · 2014Article
- Disrupting BCR-ABL in combination with secondary leukemia-specific pathways in CML cells leads to enhanced apoptosis and decreased proliferation.Molecular pharmaceutics · 2013Article
- MUC1c regulates cell survival in pancreatic cancer by preventing lysosomal permeabilization.PloS one · 2012Article
- Article
- MUC1-C oncoprotein promotes STAT3 activation in an autoinductive regulatory loop.Science signaling · 2011Article
- ABL fusion oncogene transformation and inhibitor sensitivity are mediated by the cellular regulator RIN1.Leukemia · 2011Article
- MUC1-C Oncoprotein Blocks Terminal Differentiation of Chronic Myelogenous Leukemia Cells by a ROS-Mediated Mechanism.Genes & cancer · 2011Article
- The MUC1-C oncoprotein as a target in hematologic malignancies.Cancer biology & therapy · 2010Article
- Terminal differentiation of chronic myelogenous leukemia cells is induced by targeting of the MUC1-C oncoprotein.Cancer biology & therapy · 2010Article
- Expression of a Src family kinase in chronic myelogenous leukemia cells induces resistance to imatinib in a kinase-dependent manner.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic myelogenous leukemia (CML) results from expression of the Bcr-Abl fusion protein in hematopoietic stem cells. The MUC1 heterodimeric protein is aberrantly overexpressed in diverse human carcinomas. The present studies show that MUC1 is expressed in the human K562 and KU812 CML cell lines. The results show that MUC1 associates with Bcr-Abl through a direct interaction between the Bcr N-terminal region and the MUC1 cytoplasmic domain. Stable silencing of MUC1 decreased cytoplasmic Bcr-Abl levels by promoting Bcr-Abl degradation. Silencing MUC1 was also associated with decreases in K562 and KU812 cell self-renewal capacity and with a more differentiated erythroid phenotype. The results further show that silencing MUC1 increases sensitivity of CML cells to imatinib-induced apoptosis. Analysis of primary CML blasts confirmed that, as found with the CML cell lines, MUC1 blocks differentiation and the apoptotic response to imatinib treatment. These findings indicate that MUC1 stabilizes Bcr-Abl and contributes to the pathogenesis of CML cells by promoting self renewal and inhibiting differentiation and apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.