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Article: Characterization of a novel tumor-suppressor gene PLCδ1 at 3p22 in esophageal squamous cell carcinoma

TitleCharacterization of a novel tumor-suppressor gene PLCδ1 at 3p22 in esophageal squamous cell carcinoma
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2007, v. 67 n. 22, p. 10720-10726 How to Cite?
AbstractDeletion of 3p is one of the most frequent chromosomal alterations in many solid tumors, including esophageal squamous cell carcinoma (ESCC), suggesting the existence of one or more tumor-suppressor genes at 3p. Recently, our loss of heterozygosity study revealed that 3p22 was frequently deleted in ESCC and a candidate tumor-suppressor gene (TSG), phospholipase C-δ1 (PLCδ1), was identified within the 3p22 region. In this study, absent expression of PLCδ1 was detected in 26 of 50 (52%) primary ESCCs and 4 of 9 (44.4%) ESCC cell lines, which was significantly associated with DNA copy number loss and promoter hypermethylation (P < 0.05). Functional studies showed that PLCδ1 was able to suppress both in vitro and in vivo tumorigenic ability of ESCC cells, including foci formation, colony formation in soft agar, and tumor formation in nude mice. The tumor-suppressive mechanism of PLCδ1 was associated with its role in the cell cycle arrest at the G 1-S checkpoint by up-regulation of p21 and down-regulation of phosphorylated Akt (Ser 473). In addition, down-regulation of PLCδ1 protein was significantly correlated with ESCC metastasis (P = 0.014), which was associated with its function in increasing cell adhesion and inhibiting cell mobility. Taken together, our results suggest that PLCδ1 plays an important suppressive role in the development and progression of ESCC. ©2007 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/148530
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References
Errata

 

DC FieldValueLanguage
dc.contributor.authorFu, Len_HK
dc.contributor.authorQin, YRen_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorHu, Len_HK
dc.contributor.authorKwong, DLen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorSai, WTen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2012-05-29T06:13:33Z-
dc.date.available2012-05-29T06:13:33Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer Research, 2007, v. 67 n. 22, p. 10720-10726en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148530-
dc.description.abstractDeletion of 3p is one of the most frequent chromosomal alterations in many solid tumors, including esophageal squamous cell carcinoma (ESCC), suggesting the existence of one or more tumor-suppressor genes at 3p. Recently, our loss of heterozygosity study revealed that 3p22 was frequently deleted in ESCC and a candidate tumor-suppressor gene (TSG), phospholipase C-δ1 (PLCδ1), was identified within the 3p22 region. In this study, absent expression of PLCδ1 was detected in 26 of 50 (52%) primary ESCCs and 4 of 9 (44.4%) ESCC cell lines, which was significantly associated with DNA copy number loss and promoter hypermethylation (P < 0.05). Functional studies showed that PLCδ1 was able to suppress both in vitro and in vivo tumorigenic ability of ESCC cells, including foci formation, colony formation in soft agar, and tumor formation in nude mice. The tumor-suppressive mechanism of PLCδ1 was associated with its role in the cell cycle arrest at the G 1-S checkpoint by up-regulation of p21 and down-regulation of phosphorylated Akt (Ser 473). In addition, down-regulation of PLCδ1 protein was significantly correlated with ESCC metastasis (P = 0.014), which was associated with its function in increasing cell adhesion and inhibiting cell mobility. Taken together, our results suggest that PLCδ1 plays an important suppressive role in the development and progression of ESCC. ©2007 American Association for Cancer Research.en_HK
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshCarcinoma, Squamous Cell - Genetics - Metabolismen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshChromosomes, Human, Pair 3 - Ultrastructureen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshEsophageal Neoplasms - Genetics - Metabolismen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshNeoplasm Metastasisen_US
dc.subject.meshNeoplasm Transplantationen_US
dc.subject.meshPhospholipase C Delta - Biosynthesis - Genetics - Physiologyen_US
dc.titleCharacterization of a novel tumor-suppressor gene PLCδ1 at 3p22 in esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailKwong, DL:dlwkwong@hku.hken_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityKwong, DL=rp00414en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1158/0008-5472.CAN-07-2411en_HK
dc.identifier.pmid18006814-
dc.identifier.scopuseid_2-s2.0-36349033101en_HK
dc.identifier.hkuros139056-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-36349033101&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume67en_HK
dc.identifier.issue22en_HK
dc.identifier.spage10720en_HK
dc.identifier.epage10726en_HK
dc.identifier.isiWOS:000251044000014-
dc.publisher.placeUnited Statesen_HK
dc.relation.erratumdoi:10.1158/0008-5472.CAN-68-9-COR1-
dc.identifier.scopusauthoridFu, L=12238958200en_HK
dc.identifier.scopusauthoridQin, YR=7403100680en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridHu, L=34770075600en_HK
dc.identifier.scopusauthoridKwong, DL=15744231600en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridSai, WT=6507617572en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK

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