ArticleCancer biology & therapy2010
Terminal differentiation of chronic myelogenous leukemia cells is induced by targeting of the MUC1-C oncoprotein.
Article in Cancer biology & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Inhibition of mitochondrial folate metabolism drives differentiation through mTORC1 mediated purine sensing.Nature communications · 2024Article
- Targeting MUC1-C reverses the cisplatin resistance of esophageal squamous cell carcinomaTranslational cancer research · 2021Article
- Localized fluorescent imaging of multiple proteins on individual extracellular vesicles using rolling circle amplification for cancer diagnosis.Journal of extracellular vesicles · 2020Article
- Inhibition of MUC1-C regulates metabolism by AKT pathway in esophageal squamous cell carcinoma.Journal of cellular physiology · 2019Article
- ACPred: A Computational Tool for the Prediction and Analysis of Anticancer Peptides.Molecules (Basel, Switzerland) · 2019Article
- Deletion of MBD2 inhibits proliferation of chronic myeloid leukaemia blast phase cells.Cancer biology & therapy · 2018Article
- Inhibition of MUC1-C entering nuclear suppresses MYC expression and attenuates malignant growth in esophageal squamous cell carcinoma.OncoTargets and therapy · 2018Article
- Targeting MUC1-C inhibits the AKT-S6K1-elF4A pathway regulating TIGAR translation in colorectal cancer.Molecular cancer · 2017Article
- Origin of anti-tumor activity of the cysteine-containing GO peptides and further optimization of their cytotoxic properties.Scientific reports · 2017Article
- MUC1 in hematological malignancies.Leukemia & lymphoma · 2016Review
- MUC1 (CD227): a multi-tasked molecule.Cellular and molecular life sciences : CMLS · 2015Review
- Spred2 modulates the erythroid differentiation induced by imatinib in chronic myeloid leukemia cells.PloS one · 2015Article
- Oxidative stress-induced signaling pathways implicated in the pathogenesis of Parkinson's disease.Neuromolecular medicine · 2014Review
- Identification of cell-penetrating peptides that are bactericidal to Neisseria meningitidis and prevent inflammatory responses upon infection.Antimicrobial agents and chemotherapy · 2013Article
- 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
- 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
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8 authors at 3 institutions in 1 country.
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Abstract
Chronic myelogenous leukemia (CML) is caused by expression of the Bcr-Abl fusion protein in hematopoietic stem cells. The MUC1-C oncoprotein is expressed in CML blasts and stabilizes Bcr-Abl. The present studies demonstrate that treatment of KU812 and K562 CML cells with GO-201, a cell-penetrating peptide inhibitor of MUC1-C oligomerization, downregulates Bcr-Abl expression and inhibits cell growth. In concert with decreases in Bcr-Abl levels, KU812 and K562 cells responded to GO-201 with induction of a differentiated myeloid phenotype as evidenced by increased expression of CD11b, CD11c and CD14. The results also show that the GO-201-treated cells undergo a late apoptotic/necrotic response, consistent with induction of terminal differentiation. Primary CML blasts expressing MUC1 similarly responded to GO-201 with induction of a more differentiated phenotype and late apoptosis/necrosis. In addition, treatment of KU812 xenografts in nude mice was associated with upregulation of CD11 and tumor regression. These findings indicate that CML blasts respond to targeting of the MUC1-C oncoprotein with induction of terminal differentiation.
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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.