ArticleBlood2011
MUC1-C oncoprotein suppresses reactive oxygen species-induced terminal differentiation of acute myelogenous leukemia cells.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Improved breast cancer diagnosis using a CA15-3 capture antibody-lectin sandwich assay.Breast cancer research and treatment · 2025Article
- Mucin in cancer: a stealth cloak for cancer cells.BMB reports · 2021Review
- Design, Synthesis, and Biological Evaluation of Quinazolin-4-one-Based Hydroxamic Acids as Dual PI3K/HDAC Inhibitors.Journal of medicinal chemistry · 2020Article
- Inhibition of MUC1-C regulates metabolism by AKT pathway in esophageal squamous cell carcinoma.Journal of cellular physiology · 2019Article
- MUC1-C drives myeloid leukaemogenesis and resistance to treatment by a survivin-mediated mechanism.Journal of cellular and molecular medicine · 2018Article
- Article
- MUC1-mediated induction of myeloid-derived suppressor cells in patients with acute myeloid leukemia.Blood · 2017Article
- 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-C induces DNA methyltransferase 1 and represses tumor suppressor genes in acute myeloid leukemia.Oncotarget · 2016Article
- Assessment of circulating biochemical markers and antioxidative status in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) patients.Saudi journal of biological sciences · 2015Article
- Protein mislocalization: mechanisms, functions and clinical applications in cancer.Biochimica et biophysica acta · 2014Review
- MUC1: a novel metabolic master regulator.Biochimica et biophysica acta · 2014Review
- Identification and characterization of agonist epitopes of the MUC1-C oncoprotein.Cancer immunology, immunotherapy : CII · 2014Article
- Article
- Novel roles of reactive oxygen species in the pathogenesis of acute myeloid leukemia.Journal of leukocyte biology · 2013Review
- MUC1 is a potential target for the treatment of acute myeloid leukemia stem cells.Cancer research · 2013Article
- Leukemia-associated antigens and their relevance to the immunotherapy of acute myeloid leukemia.Leukemia · 2012Review
- Targeting cysteine-mediated dimerization of the MUC1-C oncoprotein in human cancer cells.International journal of oncology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) cells are characterized by unlimited self-renewal and an impaired capacity to undergo terminal differentiation. The MUC1 oncoprotein is aberrantly expressed in AML cells; however, there has been no evidence for involvement of MUC1 in myeloid leukemogenesis. Cell-penetrating peptide inhibitors of the MUC1-C subunit block its oligomerization and thereby oncogenic function. The present results demonstrate that treatment of human MOLM-14 and MV4-11 AML cells with these inhibitors is associated with arrest of growth, induction of late apoptosis/necrosis, and loss of self-renewal capacity. Similar results were obtained with primary blasts from patients with AML. Inhibition of MUC1-C was associated with increases in reactive oxygen species (ROS) and depletion of glutathione. Increases in ROS have been linked to induction of hematopoietic cell differentiation along the myeloid lineage. In this regard, inhibition of MUC1-C was associated with induction of a terminally differentiated myeloid phenotype in AML cell lines and primary blasts by an ROS-dependent mechanism. These findings indicate that MUC1-C function is of importance to AML cell self-renewal and that inhibition of MUC1-C represents a potential therapeutic approach to induce terminal differentiation of AML cells.
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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.