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Article: TAp73-mediated the activation of C-jun N-terminal kinase enhances cellular chemosensitivity to cisplatin in ovarian cancer cells

TitleTAp73-mediated the activation of C-jun N-terminal kinase enhances cellular chemosensitivity to cisplatin in ovarian cancer cells
Authors
KeywordsCisplatin
Growth arrest and DNA damage inducible protein 45
Growth arrest and DNA damage inducible protein 45 alpha
Mitogen activated protein kinase kinase 4
Protein p73
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2012, v. 7 n. 8, article no. e42985 How to Cite?
AbstractP73, one member of the tumor suppressor p53 family, shares highly structural and functional similarity to p53. Like p53, the transcriptionally active TAp73 can mediate cellular response to chemotherapeutic agents in human cancer cells by up-regulating the expressions of its pro-apoptotic target genes such as PUMA, Bax, NOXA. Here, we demonstrated a novel molecular mechanism for TAp73-mediated apoptosis in response to cisplatin in ovarian cancer cells, and that was irrespective of p53 status. We found that TAp73 acted as an activator of the c-Jun N-terminal kinase (JNK) signaling pathway by up-regulating the expression of its target growth arrest and DNA-damage-inducible protein GADD45 alpha (GADD45alpha) and subsequently activating mitogen-activated protein kinase kinase-4 (MKK4). Inhibition of JNK activity by a specific inhibitor or small interfering RNA (siRNA) significantly abrogated TAp73-mediated apoptosis induced by cisplatin. Furthermore, inhibition of GADD45alpha by siRNA inactivated MKK4/JNK activities and also blocked TAp73-mediated apoptosis induction by cisplatin. Our study has demonstrated that TAp73 activated the JNK apoptotic signaling pathway in response to cisplatin in ovarian cancer cells.
Persistent Identifierhttp://hdl.handle.net/10722/173380
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Pen_US
dc.contributor.authorLiu, SSen_US
dc.contributor.authorNgan, HYSen_US
dc.date.accessioned2012-10-30T06:29:57Z-
dc.date.available2012-10-30T06:29:57Z-
dc.date.issued2012en_US
dc.identifier.citationPLoS One, 2012, v. 7 n. 8, article no. e42985en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://hdl.handle.net/10722/173380-
dc.description.abstractP73, one member of the tumor suppressor p53 family, shares highly structural and functional similarity to p53. Like p53, the transcriptionally active TAp73 can mediate cellular response to chemotherapeutic agents in human cancer cells by up-regulating the expressions of its pro-apoptotic target genes such as PUMA, Bax, NOXA. Here, we demonstrated a novel molecular mechanism for TAp73-mediated apoptosis in response to cisplatin in ovarian cancer cells, and that was irrespective of p53 status. We found that TAp73 acted as an activator of the c-Jun N-terminal kinase (JNK) signaling pathway by up-regulating the expression of its target growth arrest and DNA-damage-inducible protein GADD45 alpha (GADD45alpha) and subsequently activating mitogen-activated protein kinase kinase-4 (MKK4). Inhibition of JNK activity by a specific inhibitor or small interfering RNA (siRNA) significantly abrogated TAp73-mediated apoptosis induced by cisplatin. Furthermore, inhibition of GADD45alpha by siRNA inactivated MKK4/JNK activities and also blocked TAp73-mediated apoptosis induction by cisplatin. Our study has demonstrated that TAp73 activated the JNK apoptotic signaling pathway in response to cisplatin in ovarian cancer cells.en_US
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_US
dc.relation.ispartofPLoS Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCisplatin-
dc.subjectGrowth arrest and DNA damage inducible protein 45-
dc.subjectGrowth arrest and DNA damage inducible protein 45 alpha-
dc.subjectMitogen activated protein kinase kinase 4-
dc.subjectProtein p73-
dc.titleTAp73-mediated the activation of C-jun N-terminal kinase enhances cellular chemosensitivity to cisplatin in ovarian cancer cellsen_US
dc.typeArticleen_US
dc.identifier.emailLiu, SS: stephasl@hku.hken_US
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_US
dc.identifier.authorityLiu, SS=rp00372en_US
dc.identifier.authorityNgan, HYS=rp00346en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1371/journal.pone.0042985en_US
dc.identifier.pmid22900074-
dc.identifier.pmcidPMC3416758-
dc.identifier.scopuseid_2-s2.0-84864964240en_US
dc.identifier.hkuros207764-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84864964240&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume7en_US
dc.identifier.issue8, article no. e42985en_US
dc.identifier.isiWOS:000307380900092-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNgan, HYS=34571944100en_US
dc.identifier.scopusauthoridLiu, SS=37102450400en_US
dc.identifier.scopusauthoridZhang, P=55336833100en_US

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