ArticleGenes & cancer2010
MUC1-C Oncoprotein Interacts Directly with ATM and Promotes the DNA Damage Response to Ionizing Radiation.
Article in Genes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The trial behind it
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Evolution ofInternational journal of molecular sciences · 2026Review
- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- MUC1-C regulates NEAT1 lncRNA expression and paraspeckle formation in cancer progression.Oncogene · 2024Article
- XIST and MUC1-C form an auto-regulatory pathway in driving cancer progression.Cell death & disease · 2024Article
- MUC1-C is a target of salinomycin in inducing ferroptosis of cancer stem cells.Cell death discovery · 2024Article
- MUC1-C intersects chronic inflammation with epigenetic reprogramming by regulating the set1a compass complex in cancer progression.Communications biology · 2023Article
- MUC1-C Dictates PBRM1-Mediated Chronic Induction of Interferon Signaling, DNA Damage Resistance, and Immunosuppression in Triple-Negative Breast Cancer.Molecular cancer research : MCR · 2023Article
- Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non-neuroendocrine Small Cell Lung Cancer.Molecular cancer research : MCR · 2022Article
- Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression.International journal of molecular sciences · 2022Review
- Addiction of Merkel cell carcinoma to MUC1-C identifies a potential new target for treatment.Oncogene · 2022Article
- Targeting MUC1-C Suppresses Chronic Activation of Cytosolic Nucleotide Receptors and STING in Triple-Negative Breast Cancer.Cancers · 2022Article
- Article
- MUC1-C Integrates Chromatin Remodeling and PARP1 Activity in the DNA Damage Response of Triple-Negative Breast Cancer Cells.Cancer research · 2019Article
- MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- MUC1 induces acquired chemoresistance by upregulating ABCB1 in EGFR-dependent manner.Cell death & disease · 2017Article
- Mathematical modelling of phenotypic plasticity and conversion to a stem-cell state under hypoxia.Scientific reports · 2016Article
- MUC1 and MUC4: switching the emphasis from large to small.Cancer biotherapy & radiopharmaceuticals · 2011Review
- Article
- The cytoplasmic domain of MUC1 induces hyperplasia in the mammary gland and correlates with nuclear accumulation of β-catenin.PloS one · 2011Article
- Impact of MUC1 mucin downregulation in the phenotypic characteristics of MKN45 gastric carcinoma cell line.PloS one · 2011Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
The ataxia-telangiectasia mutated (ATM) kinase is activated in the cellular response to ionizing radiation (IR) and is of importance to the repair of DNA double strand breaks (DSBs). The MUC1 oncoprotein is aberrantly overexpressed in human breast carcinomas. The present work demonstrates that the MUC1 C-terminal subunit (MUC1-C) constitutively interacts with ATM in human breast cancer cells. We show that the MUC1-C cytoplasmic domain binds directly to ATM HEAT repeats. Our results also demonstrate that the MUC1-C cytoplasmic domain binds to the ATM substrate H2AX. The functional significance of these interactions is supported by the finding that MUC1-C promotes removal of IR-induced nuclear γH2AX foci. MUC1-C also protects against IR-induced chromosomal aberrations. In concert with these results, MUC1-C blocks IR-induced death by promoting repair of potentially lethal DNA damage. These findings indicate that the overexpression of MUC1 can protect against IR-induced DNA DSBs and may represent a physiologic response that has been exploited by malignant cells.
Identifiers
What OpenQuestion holds
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.