ArticleBMC cancer2014
DEK is a potential marker for aggressive phenotype and irinotecan-based therapy response in metastatic colorectal cancer.
Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Potential ofMolecular and clinical oncology · 2022Article
- Interaction of Proteins with Inverted Repeats and Cruciform Structures in Nucleic Acids.International journal of molecular sciences · 2022Review
- Inhibition of DEK Enhances Doxorubicin-Induced Apoptosis and Cell Cycle Arrest in T-Cell Acute Lymphoblastic Leukemia Cells.Disease markers · 2022Article
- DEK overexpression is predictive of poor prognosis in esophageal squamous cell carcinoma.Archives of medical science : AMS · 2021Article
- Article
- Development and validation of an individualized gene expression-based signature to predict overall survival in metastatic colorectal cancer.Annals of translational medicine · 2020Article
- UNR/Journal of clinical medicine · 2019Article
- NUP214 in Leukemia: It's More than Transport.Cells · 2019Review
- Oncogene DEK is highly expressed in lung cancerous tissues and positively regulates cell proliferation as well as invasion.Oncology letters · 2018Article
- Article
- Dek overexpression in murine epithelia increases overt esophageal squamous cell carcinoma incidence.PLoS genetics · 2018Article
- The potential predictive value of DEK expression for neoadjuvant chemoradiotherapy response in locally advanced rectal cancer.BMC cancer · 2018Article
- The nuclear DEK interactome supports multi-functionality.Proteins · 2018Article
- MicroRNA-1292-5p inhibits cell growth, migration and invasion of gastric carcinoma by targeting DEK.American journal of cancer research · 2018Article
- Prognostic role of DEK in human solid tumors: a meta-analysis.Oncotarget · 2017Article
- TFEB-VEGFA (6p21.1) co-amplified renal cell carcinoma: a distinct entity with potential implications for clinical management.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- DEK associates with tumor stage and outcome in HPV16 positive oropharyngeal squamous cell carcinoma.Oncotarget · 2017Article
- DEK is required for homologous recombination repair of DNA breaks.Scientific reports · 2017Article
- Hypoxia-induced vasculogenic mimicry formation in human colorectal cancer cells: Involvement of HIF-1a, Claudin-4, and E-cadherin and Vimentin.Scientific reports · 2016Article
- MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene.Translational oncology · 2016Article
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundDEK is a transcription factor involved in stabilization of heterochromatin and cruciform structures. It plays an important role in development and progression of different types of cancer. This study aims to analyze the role of DEK in metastatic colorectal cancer.
methodsBaseline DEK expression was firstly quantified in 9 colorectal cell lines and normal mucosa by WB. SiRNA-mediated DEK inhibition was carried out for transient DEK silencing in DLD1 and SW620 to dissect its role in colorectal cancer aggressiveness. Irinotecan response assays were performed with SN38 over 24 hours and apoptosis was quantified by flow cytometry. Ex-vivo assay was carried out with 3 fresh tumour tissues taken from surgical resection and treated with SN38 for 24 hours. DEK expression was determined by immunohistochemistry in 67 formalin-fixed paraffin-embedded tumour samples from metastatic colorectal cancer patients treated with irinotecan-based therapy as first-line treatment.
resultsThe DEK oncogene is overexpressed in all colorectal cancer cell lines. Knock-down of DEK on DLD1 and SW620 cell lines decreased cell migration and increased irinotecan-induced apoptosis. In addition, low DEK expression level predicted irinotecan-based chemotherapy response in metastatic colorectal cancer patients with KRAS wild-type.
conclusionsThese data suggest DEK overexpression as a crucial event for the emergence of an aggressive phenotype in colorectal cancer and its potential role as biomarker for irinotecan response in those patients with KRAS wild-type status.
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