DEK is a potential marker for aggressive phenotype and irinotecan-based therapy response in metastatic colorectal cancer
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...
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| Veröffentlicht in: | BMC cancer 2014-12, Vol.14 (1), p.965-965, Article 965 |
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| creator | Martinez-Useros, Javier Rodriguez-Remirez, Maria Borrero-Palacios, Aurea Moreno, Irene Cebrian, Arancha Gomez del Pulgar, Teresa del Puerto-Nevado, Laura Vega-Bravo, Ricardo Puime-Otin, Alberto Perez, Nuria Zazo, Sandra Senin, Clara Fernandez-Aceñero, Maria J Soengas, Maria S Rojo, Federico Garcia-Foncillas, Jesus |
| description | 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. |
| doi_str_mv | 10.1186/1471-2407-14-965 |
| format | Article |
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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.</description><identifier>ISSN: 1471-2407</identifier><identifier>EISSN: 1471-2407</identifier><identifier>DOI: 10.1186/1471-2407-14-965</identifier><identifier>PMID: 25515240</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Adult ; Aged ; Antineoplastic Agents, Phytogenic - therapeutic use ; Apoptosis ; Biomarkers, Tumor - analysis ; Biomarkers, Tumor - physiology ; Breast cancer ; Camptothecin - analogs & derivatives ; Camptothecin - therapeutic use ; Cell Line, Tumor ; Cell Movement ; Cell Survival ; Chemotherapy ; Chromosomal Proteins, Non-Histone - analysis ; Chromosomal Proteins, Non-Histone - physiology ; Colorectal cancer ; Colorectal Neoplasms - chemistry ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - pathology ; Down-Regulation ; Female ; Gene Expression ; Gene Knockdown Techniques ; Humans ; Irinotecan ; Male ; Medical research ; Medical treatment ; Middle Aged ; Oncogene Proteins - analysis ; Oncogene Proteins - physiology ; Phenotype ; Poly-ADP-Ribose Binding Proteins ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins p21(ras) ; ras Proteins - genetics</subject><ispartof>BMC cancer, 2014-12, Vol.14 (1), p.965-965, Article 965</ispartof><rights>2014 Martinez-Useros et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Martinez-Useros et al.; licensee BioMed Central. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b484t-2570ffad5f23fba517656027f9e3995adc60aa5d4389e68df0f5b458f9c7152e3</citedby><cites>FETCH-LOGICAL-b484t-2570ffad5f23fba517656027f9e3995adc60aa5d4389e68df0f5b458f9c7152e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4300837/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4300837/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25515240$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martinez-Useros, Javier</creatorcontrib><creatorcontrib>Rodriguez-Remirez, Maria</creatorcontrib><creatorcontrib>Borrero-Palacios, Aurea</creatorcontrib><creatorcontrib>Moreno, Irene</creatorcontrib><creatorcontrib>Cebrian, Arancha</creatorcontrib><creatorcontrib>Gomez del Pulgar, Teresa</creatorcontrib><creatorcontrib>del Puerto-Nevado, Laura</creatorcontrib><creatorcontrib>Vega-Bravo, Ricardo</creatorcontrib><creatorcontrib>Puime-Otin, Alberto</creatorcontrib><creatorcontrib>Perez, Nuria</creatorcontrib><creatorcontrib>Zazo, Sandra</creatorcontrib><creatorcontrib>Senin, Clara</creatorcontrib><creatorcontrib>Fernandez-Aceñero, Maria J</creatorcontrib><creatorcontrib>Soengas, Maria S</creatorcontrib><creatorcontrib>Rojo, Federico</creatorcontrib><creatorcontrib>Garcia-Foncillas, Jesus</creatorcontrib><title>DEK is a potential marker for aggressive phenotype and irinotecan-based therapy response in metastatic colorectal cancer</title><title>BMC cancer</title><addtitle>BMC Cancer</addtitle><description>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.</description><subject>Adult</subject><subject>Aged</subject><subject>Antineoplastic Agents, Phytogenic - therapeutic use</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Biomarkers, Tumor - physiology</subject><subject>Breast cancer</subject><subject>Camptothecin - analogs & derivatives</subject><subject>Camptothecin - therapeutic use</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Survival</subject><subject>Chemotherapy</subject><subject>Chromosomal Proteins, Non-Histone - analysis</subject><subject>Chromosomal Proteins, Non-Histone - physiology</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - chemistry</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - 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therapeutic use</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Biomarkers, Tumor - physiology</topic><topic>Breast cancer</topic><topic>Camptothecin - analogs & derivatives</topic><topic>Camptothecin - therapeutic use</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Survival</topic><topic>Chemotherapy</topic><topic>Chromosomal Proteins, Non-Histone - analysis</topic><topic>Chromosomal Proteins, Non-Histone - physiology</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - chemistry</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Irinotecan</topic><topic>Male</topic><topic>Medical research</topic><topic>Medical treatment</topic><topic>Middle Aged</topic><topic>Oncogene Proteins - analysis</topic><topic>Oncogene Proteins - physiology</topic><topic>Phenotype</topic><topic>Poly-ADP-Ribose Binding Proteins</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins p21(ras)</topic><topic>ras Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martinez-Useros, Javier</creatorcontrib><creatorcontrib>Rodriguez-Remirez, Maria</creatorcontrib><creatorcontrib>Borrero-Palacios, Aurea</creatorcontrib><creatorcontrib>Moreno, Irene</creatorcontrib><creatorcontrib>Cebrian, Arancha</creatorcontrib><creatorcontrib>Gomez del Pulgar, Teresa</creatorcontrib><creatorcontrib>del Puerto-Nevado, Laura</creatorcontrib><creatorcontrib>Vega-Bravo, Ricardo</creatorcontrib><creatorcontrib>Puime-Otin, Alberto</creatorcontrib><creatorcontrib>Perez, Nuria</creatorcontrib><creatorcontrib>Zazo, Sandra</creatorcontrib><creatorcontrib>Senin, Clara</creatorcontrib><creatorcontrib>Fernandez-Aceñero, Maria J</creatorcontrib><creatorcontrib>Soengas, Maria S</creatorcontrib><creatorcontrib>Rojo, Federico</creatorcontrib><creatorcontrib>Garcia-Foncillas, Jesus</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martinez-Useros, Javier</au><au>Rodriguez-Remirez, Maria</au><au>Borrero-Palacios, Aurea</au><au>Moreno, Irene</au><au>Cebrian, Arancha</au><au>Gomez del Pulgar, Teresa</au><au>del Puerto-Nevado, Laura</au><au>Vega-Bravo, Ricardo</au><au>Puime-Otin, Alberto</au><au>Perez, Nuria</au><au>Zazo, Sandra</au><au>Senin, Clara</au><au>Fernandez-Aceñero, Maria J</au><au>Soengas, Maria S</au><au>Rojo, Federico</au><au>Garcia-Foncillas, Jesus</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DEK is a potential marker for aggressive phenotype and irinotecan-based therapy response in metastatic colorectal cancer</atitle><jtitle>BMC cancer</jtitle><addtitle>BMC Cancer</addtitle><date>2014-12-16</date><risdate>2014</risdate><volume>14</volume><issue>1</issue><spage>965</spage><epage>965</epage><pages>965-965</pages><artnum>965</artnum><issn>1471-2407</issn><eissn>1471-2407</eissn><abstract>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.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>25515240</pmid><doi>10.1186/1471-2407-14-965</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Antineoplastic Agents, Phytogenic - therapeutic use Apoptosis Biomarkers, Tumor - analysis Biomarkers, Tumor - physiology Breast cancer Camptothecin - analogs & derivatives Camptothecin - therapeutic use Cell Line, Tumor Cell Movement Cell Survival Chemotherapy Chromosomal Proteins, Non-Histone - analysis Chromosomal Proteins, Non-Histone - physiology Colorectal cancer Colorectal Neoplasms - chemistry Colorectal Neoplasms - drug therapy Colorectal Neoplasms - pathology Down-Regulation Female Gene Expression Gene Knockdown Techniques Humans Irinotecan Male Medical research Medical treatment Middle Aged Oncogene Proteins - analysis Oncogene Proteins - physiology Phenotype Poly-ADP-Ribose Binding Proteins Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins p21(ras) ras Proteins - genetics |
| title | DEK is a potential marker for aggressive phenotype and irinotecan-based therapy response in metastatic colorectal cancer |
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