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Article: Enhancement of the radiosensitivity of cervical cancer cells by overexpressing p73α

TitleEnhancement of the radiosensitivity of cervical cancer cells by overexpressing p73α
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://mct.aacrjournals.org/
Citation
Molecular Cancer Therapeutics, 2006, v. 5 n. 5, p. 1209-1215 How to Cite?
AbstractRadiation therapy is the most effective therapy for cervical cancer in advanced stages. p53 plays a critical role in the cellular response to radiation-induced DNA damage. However, p53 function is often impaired in the presence of the oncoprotein E6 from human papillomavirus, which is often associated with the development of cervical cancer. p73, a p53 family member, is highly similar to p53, but is resistant to the degradation by human papillomavirus E6. In this study, we investigated the role of p73α in relation to cellular radiosensitivity in the p53-impaired cervical cancer cells. Radiosensitivity and irradiation-induced apoptotic cell death were examined in the exogenous overexpressed p73α- and p53-impaired cells. Our results showed that the endogenous p73α expressed only in the radiosensitive cervical cancer C4-1 cells, but not in the radioresistant SiHa, Caski, and HeLa cells. Overexpression of exogenous p73α by transfection in the radioresistant cells resulted in a significant increase of cellular sensitivity to radiation. Enhanced radiosensitivity in p73α-transfected cells was attributed by increase of cellular apoptosis. Coactivation of p21 was also observed in the p73α-transfected cells upon radiation treatment. In summary, our findings suggested that p73α is an important determinant of cellular radiosensitivity in the p53-impaired cervical cancer cells. Copyright © 2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/148467
ISSN
2015 Impact Factor: 5.579
2015 SCImago Journal Rankings: 3.224
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, SSen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorLeung, RCYen_HK
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorLeung, TWen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2012-05-29T06:13:08Z-
dc.date.available2012-05-29T06:13:08Z-
dc.date.issued2006en_HK
dc.identifier.citationMolecular Cancer Therapeutics, 2006, v. 5 n. 5, p. 1209-1215en_HK
dc.identifier.issn1535-7163en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148467-
dc.description.abstractRadiation therapy is the most effective therapy for cervical cancer in advanced stages. p53 plays a critical role in the cellular response to radiation-induced DNA damage. However, p53 function is often impaired in the presence of the oncoprotein E6 from human papillomavirus, which is often associated with the development of cervical cancer. p73, a p53 family member, is highly similar to p53, but is resistant to the degradation by human papillomavirus E6. In this study, we investigated the role of p73α in relation to cellular radiosensitivity in the p53-impaired cervical cancer cells. Radiosensitivity and irradiation-induced apoptotic cell death were examined in the exogenous overexpressed p73α- and p53-impaired cells. Our results showed that the endogenous p73α expressed only in the radiosensitive cervical cancer C4-1 cells, but not in the radioresistant SiHa, Caski, and HeLa cells. Overexpression of exogenous p73α by transfection in the radioresistant cells resulted in a significant increase of cellular sensitivity to radiation. Enhanced radiosensitivity in p73α-transfected cells was attributed by increase of cellular apoptosis. Coactivation of p21 was also observed in the p73α-transfected cells upon radiation treatment. In summary, our findings suggested that p73α is an important determinant of cellular radiosensitivity in the p53-impaired cervical cancer cells. Copyright © 2006 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://mct.aacrjournals.org/en_HK
dc.relation.ispartofMolecular Cancer Therapeuticsen_HK
dc.subject.meshApoptosis - Physiology - Radiation Effectsen_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P21 - Metabolismen_US
dc.subject.meshDna-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation, Neoplastic - Radiation Effectsen_US
dc.subject.meshGenes, Tumor Suppressoren_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshNuclear Proteins - Genetics - Metabolismen_US
dc.subject.meshRadiation Tolerance - Genetics - Physiologyen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshTumor Suppressor Proteinsen_US
dc.subject.meshUterine Cervical Neoplasms - Metabolismen_US
dc.titleEnhancement of the radiosensitivity of cervical cancer cells by overexpressing p73αen_HK
dc.typeArticleen_HK
dc.identifier.emailLiu, SS: stephasl@hku.hken_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityLiu, SS=rp00372en_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1158/1535-7163.MCT-05-0451en_HK
dc.identifier.pmid16731753en_HK
dc.identifier.scopuseid_2-s2.0-33745095580en_HK
dc.identifier.hkuros116543-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745095580&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1209en_HK
dc.identifier.epage1215en_HK
dc.identifier.isiWOS:000238073800014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLiu, SS=37102450400en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridLeung, RCY=7101876103en_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridLeung, TW=36823439400en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK

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