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Article: Evidence of a novel antiapoptotic factor: Role of inhibitor of differentiation or DNA binding (Id-1) in anticancer drug-induced apoptosis

TitleEvidence of a novel antiapoptotic factor: Role of inhibitor of differentiation or DNA binding (Id-1) in anticancer drug-induced apoptosis
Authors
Issue Date2007
PublisherBlackwell Publishing Japan. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CAS
Citation
Cancer Science, 2007, v. 98 n. 3, p. 308-314 How to Cite?
AbstractId-1 (inhibitor of differentiation or DNA binding), a member of the basic helix-loop-helix transcription factor family, is up-regulated in many types of human cancer and its expression levels are correlated with poor treatment outcome and shorter survival. In this study, we provided evidence to suggest that Id-1 is a universal survival factor that plays a key role in protection against anticancer drug-induced apoptosis. Using nine anticancer drugs and five cancer cell lines derived from nasopharyngeal carcinoma (CNE1), cervical carcinoma (HeLa), breast cancer (MCF7), hepatocarcinoma (Huh7) and prostate cancer (PC3), we found that down-regulation of Id-1 expression at both transcriptional and protein levels was associated with increased apoptosis rates and increased cleaved PARP after exposure to all anticancer agents. Treatment with a caspase 9 inhibitor, Z-LEHD-FMK, protected cancer cells from drug-induced PARP cleavage. However, overexpression of Id-1 in a p53 mutated cell line, CNE1, was able to suppress PARP cleavage in response to all anticancer drugs examined. In contrast, down-regulation of Id-1 through small RNA technology in CNE1 cells led to increased sensitivity to all six types of chemotherapeutic drugs. Our results demonstrate that Id-1 may be a general negative regulator of anticancer drug-induced apoptosis and suggest a novel therapeutic target in inducing chemosensitization in cancer cells. Our evidence also provides a possible underlying mechanism responsible for the positive role of Id-1 in the progression of human cancer. © 2007 Japanese Cancer Association.
Persistent Identifierhttp://hdl.handle.net/10722/67726
ISSN
2015 Impact Factor: 3.896
2015 SCImago Journal Rankings: 1.744
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-06T05:57:42Z-
dc.date.available2010-09-06T05:57:42Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer Science, 2007, v. 98 n. 3, p. 308-314en_HK
dc.identifier.issn1347-9032en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67726-
dc.description.abstractId-1 (inhibitor of differentiation or DNA binding), a member of the basic helix-loop-helix transcription factor family, is up-regulated in many types of human cancer and its expression levels are correlated with poor treatment outcome and shorter survival. In this study, we provided evidence to suggest that Id-1 is a universal survival factor that plays a key role in protection against anticancer drug-induced apoptosis. Using nine anticancer drugs and five cancer cell lines derived from nasopharyngeal carcinoma (CNE1), cervical carcinoma (HeLa), breast cancer (MCF7), hepatocarcinoma (Huh7) and prostate cancer (PC3), we found that down-regulation of Id-1 expression at both transcriptional and protein levels was associated with increased apoptosis rates and increased cleaved PARP after exposure to all anticancer agents. Treatment with a caspase 9 inhibitor, Z-LEHD-FMK, protected cancer cells from drug-induced PARP cleavage. However, overexpression of Id-1 in a p53 mutated cell line, CNE1, was able to suppress PARP cleavage in response to all anticancer drugs examined. In contrast, down-regulation of Id-1 through small RNA technology in CNE1 cells led to increased sensitivity to all six types of chemotherapeutic drugs. Our results demonstrate that Id-1 may be a general negative regulator of anticancer drug-induced apoptosis and suggest a novel therapeutic target in inducing chemosensitization in cancer cells. Our evidence also provides a possible underlying mechanism responsible for the positive role of Id-1 in the progression of human cancer. © 2007 Japanese Cancer Association.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Japan. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CASen_HK
dc.relation.ispartofCancer Scienceen_HK
dc.subject.meshAntineoplastic Agents - therapeutic useen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshBreast Neoplasms - pathologyen_HK
dc.subject.meshCarcinoma, Hepatocellular - pathologyen_HK
dc.subject.meshCatechin - analogs & derivatives - therapeutic useen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Survival - drug effectsen_HK
dc.subject.meshCisplatin - therapeutic useen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshDoxorubicin - therapeutic useen_HK
dc.subject.meshEtoposide - therapeutic useen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHeLa Cellsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitor of Differentiation Protein 1 - metabolism - physiologyen_HK
dc.subject.meshLiver Neoplasms - pathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMechlorethamine - therapeutic useen_HK
dc.subject.meshMethotrexate - therapeutic useen_HK
dc.subject.meshMitomycin - therapeutic useen_HK
dc.subject.meshNasopharyngeal Neoplasms - pathologyen_HK
dc.subject.meshPaclitaxel - therapeutic useen_HK
dc.subject.meshProstatic Neoplasms - pathologyen_HK
dc.subject.meshVincristine - therapeutic useen_HK
dc.titleEvidence of a novel antiapoptotic factor: Role of inhibitor of differentiation or DNA binding (Id-1) in anticancer drug-induced apoptosisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1347-9032&volume=98&issue=3&spage=308&epage=314&date=2007&atitle=Evidence+of+a+novel+antiapoptotic+factor:+Role+of+inhibitor+of+differentiation+or+DNA+binding+(Id-1)+in+anticancer+drug-induced+apoptosisen_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1349-7006.2007.00400.xen_HK
dc.identifier.pmid17214747-
dc.identifier.scopuseid_2-s2.0-33846705491en_HK
dc.identifier.hkuros147705en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846705491&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume98en_HK
dc.identifier.issue3en_HK
dc.identifier.spage308en_HK
dc.identifier.epage314en_HK
dc.identifier.isiWOS:000243699700007-
dc.publisher.placeJapanen_HK
dc.identifier.scopusauthoridZhang, X=8578540900en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.citeulike1075078-

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