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Article: The role of Pea3 group transcription factors in esophageal squamous cell carcinoma

TitleThe role of Pea3 group transcription factors in esophageal squamous cell carcinoma
Authors
KeywordsApoptosis
Cancer growth
Cancer inhibition
Cancer invasion
Cancer resistance
Issue Date2011
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 2011, v. 179 n. 2, p. 992-1003 How to Cite?
Abstract
The transcription factors Pea3, Erm, and Er81 can promote cancer initiation and progression in various types of solid tumors. However, their role in esophageal squamous cell carcinoma (ESCC) has not been elucidated. In this study, we found that the expression levels of Pea3 and Erm, but not that of Er81, were significantly higher in ESCC compared with nontumor esophageal epithelium. A high level of Pea3 expression was significantly correlated with a shorter overall survival in a cohort of 81 patients with ESCC and the subgroup with N1 stage tumor (Wilcoxon-Gehan test, P = 0.016 and P = 0.001, respectively). Pea3 was overexpressed in seven ESCC cell lines compared with two immortalized esophageal cell lines. Pea3 knockdown reduced cell proliferation and suppressed nonadherent growth, migration, and invasion in ESCC cells in vitro. In addition, Pea3 knockdown in ESCC cells resulted in a down-regulation of phospho-Akt and matrix metalloproteinase 13, whereas a significant positive correlation in the expression levels was observed between Pea3 and phospho-Akt (r = 0.281, P < 0.013) and between Pea3 and matrix metalloproteinase 13 in the human specimens (r = 0.462, P < 0.001). Moreover, Pea3 modulated the sensitivity of EC109 cells to doxorubicin, probably via reduced activity of the phosphatidylinositol 3-kinaseAktmammalian target of Rapamycin complex 1 pathway on Pea3 knockdown. In conclusion, our results suggest that Pea3 plays an important role in the progression of ESCC. © 2011 American Society for Investigative Pathology.
Persistent Identifierhttp://hdl.handle.net/10722/137634
ISSN
2013 Impact Factor: 4.602
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Cancer Research UK
Funding Information:

Supported by a postdoctoral fellowship from Cancer Research UK (H.-F.Y.).

References

 

Author Affiliations
  1. The University of Hong Kong
  2. Queen's University Belfast
DC FieldValueLanguage
dc.contributor.authorYuen, HFen_HK
dc.contributor.authorMcCrudden, CMen_HK
dc.contributor.authorChan, KKen_HK
dc.contributor.authorChan, YPen_HK
dc.contributor.authorWong, MLYen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorLappin, TRen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorElTanani, Men_HK
dc.date.accessioned2011-08-26T14:29:51Z-
dc.date.available2011-08-26T14:29:51Z-
dc.date.issued2011en_HK
dc.identifier.citationAmerican Journal Of Pathology, 2011, v. 179 n. 2, p. 992-1003en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137634-
dc.description.abstractThe transcription factors Pea3, Erm, and Er81 can promote cancer initiation and progression in various types of solid tumors. However, their role in esophageal squamous cell carcinoma (ESCC) has not been elucidated. In this study, we found that the expression levels of Pea3 and Erm, but not that of Er81, were significantly higher in ESCC compared with nontumor esophageal epithelium. A high level of Pea3 expression was significantly correlated with a shorter overall survival in a cohort of 81 patients with ESCC and the subgroup with N1 stage tumor (Wilcoxon-Gehan test, P = 0.016 and P = 0.001, respectively). Pea3 was overexpressed in seven ESCC cell lines compared with two immortalized esophageal cell lines. Pea3 knockdown reduced cell proliferation and suppressed nonadherent growth, migration, and invasion in ESCC cells in vitro. In addition, Pea3 knockdown in ESCC cells resulted in a down-regulation of phospho-Akt and matrix metalloproteinase 13, whereas a significant positive correlation in the expression levels was observed between Pea3 and phospho-Akt (r = 0.281, P < 0.013) and between Pea3 and matrix metalloproteinase 13 in the human specimens (r = 0.462, P < 0.001). Moreover, Pea3 modulated the sensitivity of EC109 cells to doxorubicin, probably via reduced activity of the phosphatidylinositol 3-kinaseAktmammalian target of Rapamycin complex 1 pathway on Pea3 knockdown. In conclusion, our results suggest that Pea3 plays an important role in the progression of ESCC. © 2011 American Society for Investigative Pathology.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.subjectApoptosis-
dc.subjectCancer growth-
dc.subjectCancer inhibition-
dc.subjectCancer invasion-
dc.subjectCancer resistance-
dc.titleThe role of Pea3 group transcription factors in esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9440&volume=179&issue=2&spage=992&epage=1003&date=2011&atitle=The+role+of+pea3+group+transcription+factors+in+esophageal+squamous+cell+carcinomaen_US
dc.identifier.emailKhoo, US: uskhoo@hkucc.hku.hken_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailSrivastava, G: gopesh@pathology.hku.hken_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ajpath.2011.04.004en_HK
dc.identifier.pmid21689625en_HK
dc.identifier.pmcidPMC3157177-
dc.identifier.scopuseid_2-s2.0-80052485012en_HK
dc.identifier.hkuros191693en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80052485012&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume179en_HK
dc.identifier.issue2en_HK
dc.identifier.spage992en_HK
dc.identifier.epage1003en_HK
dc.identifier.eissn1525-2191-
dc.identifier.isiWOS:000298307200043-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYuen, HF=14018633400en_HK
dc.identifier.scopusauthoridMcCrudden, CM=16402813600en_HK
dc.identifier.scopusauthoridChan, KK=8986914100en_HK
dc.identifier.scopusauthoridChan, YP=14009821700en_HK
dc.identifier.scopusauthoridWong, MLY=37021112700en_HK
dc.identifier.scopusauthoridChan, KYK=36989360800en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridLappin, TR=7005921502en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridElTanani, M=6602759648en_HK

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