2026-07-21T09:56:02Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/254242025-12-18T13:00:09Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Martinez-Useros, Javier
author
Rodriguez-Remirez, Maria
author
Borrero-Palacios, Aurea
author
Moreno, Irene
author
Cebrian, Arancha
author
Gomez del Pulgar, Teresa
author
del Puerto-Nevado, Laura
author
Vega-Bravo, Ricardo
author
Puime-Otin, Alberto
author
Perez, Nuria
author
Zazo, Sandra
author
Senin, Clara
author
Fernandez-Aceñero, Maria J
author
Soengas, MS
author
Rojo, Federico
author
Garcia-Foncillas, Jesus
funder
Instituto de Salud Carlos III
2024-11-04T13:07:48Z
2024-11-04T13:07:48Z
2014-12-16
BMC Cancer . 2014 Dec 16:14:965.
BMC Cancer
25515240
https://hdl.handle.net/20.500.12105/25424
DEK 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.Baseline 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.The 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.These 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.
eng
DEK
Irinotecan
Aggressive phenotype
Metastatic colorectal cancer
KRAS
DEK is a potential marker for aggressive phenotype and irinotecan-based therapy response in metastatic colorectal cancer.
research article
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URL
https://repisalud.isciii.es/bitstreams/a8b3d40d-8b65-4c75-bd09-842e9ff29ce4/download
File
MD5
022f5037a414a7144eaf3f845ccdd03a
2152547
application/pdf
DEKisapotentialmarke-2014.pdf