ArticleOncogene2011
The human DEK oncogene stimulates β-catenin signaling, invasion and mammosphere formation in breast cancer.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 98 citations in OpenAlex.
- DEK Loss Induces Task-specific Deficits in Learning and Memory and Reprograms the Hippocampal Transcriptome in Mice.Molecular neurobiology · 2026Article
- All hands on DEK: structural insights into a unique histone modifier and chromatin remodeler.Epigenetics & chromatin · 2026Review
- Dek Loss Induces Sex-Dependent, Task-Specific Cognitive Deficits and Reprograms the Hippocampal Transcriptome in Mice.Research square · 2025Article
- DEK promotes mammary hyperplasia and is associated with H3K27me3 epigenetic modifications.Life science alliance · 2025Article
- DEK regulates B-cell proliferative capacity and is associated with aggressive disease in low-grade B-cell lymphomas.Blood cancer journal · 2024Article
- Single-cell transcriptomics enable the characterization of local extension in retinoblastoma.Communications biology · 2024Article
- Super-resolution microscopy reveals the nanoscale cluster architecture of the DEK protein cancer biomarker.iScience · 2023Article
- Imaging-based study demonstrates how the DEK nanoscale distribution differentially correlates with epigenetic marks in a breast cancer model.Scientific reports · 2023Article
- The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia.Experimental hematology · 2023Review
- In silico gene expression and pathway analysis of DEK in the human brain across the lifespan.The European journal of neuroscience · 2022Article
- Potential ofMolecular and clinical oncology · 2022Article
- Long Non-Coding LEF1-AS1 Sponge miR-5100 Regulates Apoptosis and Autophagy in Gastric Cancer Cells via the miR-5100/DEK/AMPK-mTOR Axis.International journal of molecular sciences · 2022Article
- Novel molecular mechanisms in Alzheimer's disease: The potential role of DEK in disease pathogenesis.Frontiers in aging neuroscience · 2022Review
- Article
- DEK is highly expressed in breast cancer and is associated with malignant phenotype and progression.Oncology letters · 2021Article
- Tumor cell intrinsic RON signaling suppresses innate immune responses in breast cancer through inhibition of IRAK4 signaling.Cancer letters · 2021Article
- Circular RNA circ_0000039 enhances gastric cancer progression through miR-1292-5p/DEK axis.Cancer biomarkers : section A of Disease markers · 2021Article
- Sevoflurane Limits Glioma Progression by Regulating Cell Proliferation, Apoptosis, Migration, and Invasion via miR-218-5p/DEK/β-Catenin Axis in Glioma.Cancer management and research · 2021Article
- Role of the DEK oncogene in the development of squamous cell carcinoma.International journal of clinical oncology · 2020Review
- DEK Expression in Breast Cancer Cells Leads to the Alternative Activation of Tumor Associated Macrophages.Cancers · 2020Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancer is a major cause of cancer-related deaths in American women; therefore, the identification of novel breast cancer-related molecules for the discovery of new markers and drug targets remains essential. The human DEK gene, which encodes a chromatin-binding protein and DNA topology regulator, is upregulated in many types of cancer. DEK has been implicated as an oncogene in breast cancer based on mRNA expression studies, but its functional significance in breast cancer growth and progression has not yet been tested directly. We demonstrate that DEK is highly expressed in breast cancer cells compared with normal tissue, and functionally important for cellular growth, invasion and mammosphere formation. DEK overexpression in non-tumorigenic MCF10A cells resulted in increased growth and motility, with a concomitant downregulation of E-cadherin. Conversely, DEK knockdown in MCF7 and MDA-MB-468 breast cancer cells resulted in decreased growth and motility with upregulation of E-cadherin. The use of DEK-proficient and -deficient breast cancer cells in orthotopic xenografts provided further in vivo evidence that DEK contributes to tumor growth. Activation of the β-catenin signaling pathway is important for normal and cancer stem cell character, growth and metastasis. We show that DEK expression stimulated, and DEK knockdown repressed β-catenin nuclear translocation and activity. Importantly, the expression of constitutively active β-catenin rescued breast cancer invasion defects of DEK knockdown cells. Together, our data indicate that DEK expression stimulates the growth, stem cell character and motility of breast cancer cells, and that DEK-dependent cellular invasion occurs at least in part via β-catenin activation.
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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.