File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Frequent decreased expression of candidate tumor suppressor gene, DEC1, and its anchorage-independent growth properties and impact on global gene expression in esophageal carcinoma
  • Basic View
  • Metadata View
  • XML View
TitleFrequent decreased expression of candidate tumor suppressor gene, DEC1, and its anchorage-independent growth properties and impact on global gene expression in esophageal carcinoma
 
AuthorsLeung, ACC6
Wong, VCL6
Li, CY6
Pui, LC6
Daigo, Y5
Nakamura, Y5
Qi, RZ6
Miller, LD4
Liu, ETB4
Li, DW3
Li, JL1
Law, S2
Sai, WT2
Lung, ML6
 
KeywordsAnchorage-independent growth
DEC1
Esophageal carcinoma
Tumor suppression
 
Issue Date2008
 
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
CitationInternational Journal Of Cancer, 2008, v. 122 n. 3, p. 587-594 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.23144
 
AbstractPrevious studies showed that expression of the novel candidate tumor suppressor gene, DEC1 (Deleted in Esophageal Cancer 1), is reduced in esophageal carcinoma and suppresses cancer cell growth in vitro and tumor growth in vivo in nude mice. This study shows that DEC1 gene expression was downregulated in 100% of 16 esophageal squamous cell carcinoma (ESCC) cell lines and 52 and 45%, respectively, of esophageal tumor specimens from Hong Kong and a high-risk ESCC region of Henan, China. Using epitope tagging, the DEC1 protein was localized to both the cytoplasm and nucleus of the cell. In 3D Matrigel culture, no significant difference in colony numbers formed was observed for DEC1 stable transfectants, as compared to vector-alone transfectant controls. However, significantly smaller colony sizes were observed for the DEC1 transfectants. In in vitro cell migration, invasion and soft agar assays of DEC1 transfectants, only the soft agar assay showed statistically significant differences in colony numbers with the vector-alone controls, indicating that DEC1 may be involved in anchorage-independent cell growth. In addition, the global gene expression affected by DEC1 in tumor-suppressive stable transfectants was investigated using cDNA oligonucleotide microarray hybridization. Three candidate genes, TFP1-2, GDF15 and DUSP6, were identified through this approach; they are downregulated in tumor segregants of DEC1 stable transfectants, ESCC cell lines and esophageal tumors and have a potential role in tumor growth and progression. These studies show that DEC1 is involved in esophageal cancer development and help elucidate its functional role in tumor development. © 2007 Wiley-Liss, Inc.
 
ISSN0020-7136
2013 Impact Factor: 5.007
 
DOIhttp://dx.doi.org/10.1002/ijc.23144
 
ISI Accession Number IDWOS:000252132900014
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLeung, ACC
 
dc.contributor.authorWong, VCL
 
dc.contributor.authorLi, CY
 
dc.contributor.authorPui, LC
 
dc.contributor.authorDaigo, Y
 
dc.contributor.authorNakamura, Y
 
dc.contributor.authorQi, RZ
 
dc.contributor.authorMiller, LD
 
dc.contributor.authorLiu, ETB
 
dc.contributor.authorLi, DW
 
dc.contributor.authorLi, JL
 
dc.contributor.authorLaw, S
 
dc.contributor.authorSai, WT
 
dc.contributor.authorLung, ML
 
dc.date.accessioned2010-09-06T05:55:33Z
 
dc.date.available2010-09-06T05:55:33Z
 
dc.date.issued2008
 
dc.description.abstractPrevious studies showed that expression of the novel candidate tumor suppressor gene, DEC1 (Deleted in Esophageal Cancer 1), is reduced in esophageal carcinoma and suppresses cancer cell growth in vitro and tumor growth in vivo in nude mice. This study shows that DEC1 gene expression was downregulated in 100% of 16 esophageal squamous cell carcinoma (ESCC) cell lines and 52 and 45%, respectively, of esophageal tumor specimens from Hong Kong and a high-risk ESCC region of Henan, China. Using epitope tagging, the DEC1 protein was localized to both the cytoplasm and nucleus of the cell. In 3D Matrigel culture, no significant difference in colony numbers formed was observed for DEC1 stable transfectants, as compared to vector-alone transfectant controls. However, significantly smaller colony sizes were observed for the DEC1 transfectants. In in vitro cell migration, invasion and soft agar assays of DEC1 transfectants, only the soft agar assay showed statistically significant differences in colony numbers with the vector-alone controls, indicating that DEC1 may be involved in anchorage-independent cell growth. In addition, the global gene expression affected by DEC1 in tumor-suppressive stable transfectants was investigated using cDNA oligonucleotide microarray hybridization. Three candidate genes, TFP1-2, GDF15 and DUSP6, were identified through this approach; they are downregulated in tumor segregants of DEC1 stable transfectants, ESCC cell lines and esophageal tumors and have a potential role in tumor growth and progression. These studies show that DEC1 is involved in esophageal cancer development and help elucidate its functional role in tumor development. © 2007 Wiley-Liss, Inc.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationInternational Journal Of Cancer, 2008, v. 122 n. 3, p. 587-594 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.23144
 
dc.identifier.doihttp://dx.doi.org/10.1002/ijc.23144
 
dc.identifier.epage594
 
dc.identifier.hkuros139681
 
dc.identifier.isiWOS:000252132900014
 
dc.identifier.issn0020-7136
2013 Impact Factor: 5.007
 
dc.identifier.issue3
 
dc.identifier.openurl
 
dc.identifier.pmid17943723
 
dc.identifier.scopuseid_2-s2.0-37349107523
 
dc.identifier.spage587
 
dc.identifier.urihttp://hdl.handle.net/10722/67486
 
dc.identifier.volume122
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
dc.publisher.placeUnited States
 
dc.relation.ispartofInternational Journal of Cancer
 
dc.relation.referencesReferences in Scopus
 
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.
 
dc.subject.meshCarcinoma, Squamous Cell - genetics - metabolism - pathology
 
dc.subject.meshCell Movement
 
dc.subject.meshEpithelium - metabolism - pathology
 
dc.subject.meshEsophageal Neoplasms - genetics - metabolism - pathology
 
dc.subject.meshFemale
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshGene Expression Regulation, Neoplastic
 
dc.subject.meshHumans
 
dc.subject.meshMale
 
dc.subject.meshMiddle Aged
 
dc.subject.meshNeoplasm Invasiveness - pathology
 
dc.subject.meshOligonucleotide Array Sequence Analysis
 
dc.subject.meshTumor Markers, Biological - genetics - metabolism
 
dc.subject.meshTumor Suppressor Proteins - genetics - metabolism
 
dc.subjectAnchorage-independent growth
 
dc.subjectDEC1
 
dc.subjectEsophageal carcinoma
 
dc.subjectTumor suppression
 
dc.titleFrequent decreased expression of candidate tumor suppressor gene, DEC1, and its anchorage-independent growth properties and impact on global gene expression in esophageal carcinoma
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Leung, ACC</contributor.author>
<contributor.author>Wong, VCL</contributor.author>
<contributor.author>Li, CY</contributor.author>
<contributor.author>Pui, LC</contributor.author>
<contributor.author>Daigo, Y</contributor.author>
<contributor.author>Nakamura, Y</contributor.author>
<contributor.author>Qi, RZ</contributor.author>
<contributor.author>Miller, LD</contributor.author>
<contributor.author>Liu, ETB</contributor.author>
<contributor.author>Li, DW</contributor.author>
<contributor.author>Li, JL</contributor.author>
<contributor.author>Law, S</contributor.author>
<contributor.author>Sai, WT</contributor.author>
<contributor.author>Lung, ML</contributor.author>
<date.accessioned>2010-09-06T05:55:33Z</date.accessioned>
<date.available>2010-09-06T05:55:33Z</date.available>
<date.issued>2008</date.issued>
<identifier.citation>International Journal Of Cancer, 2008, v. 122 n. 3, p. 587-594</identifier.citation>
<identifier.issn>0020-7136</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/67486</identifier.uri>
<description.abstract>Previous studies showed that expression of the novel candidate tumor suppressor gene, DEC1 (Deleted in Esophageal Cancer 1), is reduced in esophageal carcinoma and suppresses cancer cell growth in vitro and tumor growth in vivo in nude mice. This study shows that DEC1 gene expression was downregulated in 100% of 16 esophageal squamous cell carcinoma (ESCC) cell lines and 52 and 45%, respectively, of esophageal tumor specimens from Hong Kong and a high-risk ESCC region of Henan, China. Using epitope tagging, the DEC1 protein was localized to both the cytoplasm and nucleus of the cell. In 3D Matrigel culture, no significant difference in colony numbers formed was observed for DEC1 stable transfectants, as compared to vector-alone transfectant controls. However, significantly smaller colony sizes were observed for the DEC1 transfectants. In in vitro cell migration, invasion and soft agar assays of DEC1 transfectants, only the soft agar assay showed statistically significant differences in colony numbers with the vector-alone controls, indicating that DEC1 may be involved in anchorage-independent cell growth. In addition, the global gene expression affected by DEC1 in tumor-suppressive stable transfectants was investigated using cDNA oligonucleotide microarray hybridization. Three candidate genes, TFP1-2, GDF15 and DUSP6, were identified through this approach; they are downregulated in tumor segregants of DEC1 stable transfectants, ESCC cell lines and esophageal tumors and have a potential role in tumor growth and progression. These studies show that DEC1 is involved in esophageal cancer development and help elucidate its functional role in tumor development. &#169; 2007 Wiley-Liss, Inc.</description.abstract>
<language>eng</language>
<publisher>John Wiley &amp; Sons, Inc.. The Journal&apos;s web site is located at http://www3.interscience.wiley.com/journal/29331/home</publisher>
<relation.ispartof>International Journal of Cancer</relation.ispartof>
<rights>International Journal of Cancer. Copyright &#169; John Wiley &amp; Sons, Inc.</rights>
<subject>Anchorage-independent growth</subject>
<subject>DEC1</subject>
<subject>Esophageal carcinoma</subject>
<subject>Tumor suppression</subject>
<subject.mesh>Carcinoma, Squamous Cell - genetics - metabolism - pathology</subject.mesh>
<subject.mesh>Cell Movement</subject.mesh>
<subject.mesh>Epithelium - metabolism - pathology</subject.mesh>
<subject.mesh>Esophageal Neoplasms - genetics - metabolism - pathology</subject.mesh>
<subject.mesh>Female</subject.mesh>
<subject.mesh>Gene Expression Profiling</subject.mesh>
<subject.mesh>Gene Expression Regulation, Neoplastic</subject.mesh>
<subject.mesh>Humans</subject.mesh>
<subject.mesh>Male</subject.mesh>
<subject.mesh>Middle Aged</subject.mesh>
<subject.mesh>Neoplasm Invasiveness - pathology</subject.mesh>
<subject.mesh>Oligonucleotide Array Sequence Analysis</subject.mesh>
<subject.mesh>Tumor Markers, Biological - genetics - metabolism</subject.mesh>
<subject.mesh>Tumor Suppressor Proteins - genetics - metabolism</subject.mesh>
<title>Frequent decreased expression of candidate tumor suppressor gene, DEC1, and its anchorage-independent growth properties and impact on global gene expression in esophageal carcinoma</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0020-7136&amp;volume=122&amp;issue=3&amp;spage=587&amp;epage=594&amp;date=2008&amp;atitle=Frequent+decreased+expression+of+candidate+tumor+suppressor+gene,+DEC1,+and+its+anchorage-independent+growth+properties+and+impact+on+global+gene+expression+in+esophageal+carcinoma</identifier.openurl>
<description.nature>link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1002/ijc.23144</identifier.doi>
<identifier.pmid>17943723</identifier.pmid>
<identifier.scopus>eid_2-s2.0-37349107523</identifier.scopus>
<identifier.hkuros>139681</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-37349107523&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>122</identifier.volume>
<identifier.issue>3</identifier.issue>
<identifier.spage>587</identifier.spage>
<identifier.epage>594</identifier.epage>
<identifier.isi>WOS:000252132900014</identifier.isi>
<publisher.place>United States</publisher.place>
</item>
Author Affiliations
  1. Yaocun Esophageal Cancer Hospital
  2. The University of Hong Kong
  3. Zhengzhou University
  4. Genome Institute of Singapore
  5. Institute of Medical Science The University of Tokyo
  6. Hong Kong University of Science and Technology