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Article: Induction of mutant p53-dependent apoptosis in human hepatocellular carcinoma by targeting stress protein mortalin
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TitleInduction of mutant p53-dependent apoptosis in human hepatocellular carcinoma by targeting stress protein mortalin
 
AuthorsLu, WJ1
Lee, NP1
Kaul, SC3
Lan, F2
Poon, RTP1
Wadhwa, R3
Luk, JM4 1
 
Keywordshuman hepatocellular carcinoma
mortalin
mutant p53-dependent apoptosis
RNAi
therapy
 
Issue Date2011
 
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
CitationInternational Journal Of Cancer, 2011, v. 129 n. 8, p. 1806-1814 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.25857
 
AbstractStress protein mortalin (mtHSP70) is highly expressed in cancer cells. It was shown to contribute to carcinogenesis by sequestrating the wild type p53, a key tumor suppressor protein, in the cytoplasm resulting in an abrogation of its transcriptional activation function. We have found that the level of mortalin expression has significant correlation with human hepatocellular carcinoma (HCC) malignancy and therefore investigated whether it interacts with and influences the activities of mutant p53, frequently associated with HCC development. We have detected mortalin-p53 interactions in liver tumor and five HCC cell lines that harbored mutant p53. The data was in contrast to the normal liver and immortalized normal hepatocytes that lacked mortalin-p53 interaction. Furthermore, we have found that the shRNA-mediated mortalin silencing could induce mutant p53-mediated tumor-specific apoptosis in HCC. Such allotment of apoptotic function to mutant p53 by targeting mortalin-p53 interaction in cancer cells is a promising strategy for HCC therapy. Copyright © 2010 UICC.
 
ISSN0020-7136
2013 Impact Factor: 5.007
 
DOIhttp://dx.doi.org/10.1002/ijc.25857
 
ISI Accession Number IDWOS:000294224300002
Funding AgencyGrant Number
The HKU CRCG
New Energy & Industrial Technology Development Organization (NEDO)
Funding Information:

Grant sponsors: The HKU CRCG seed fund, New Energy & Industrial Technology Development Organization (NEDO) and Grant-in-Aid for Japan Society for the Promotion of Science (JSPS), Japan

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLu, WJ
 
dc.contributor.authorLee, NP
 
dc.contributor.authorKaul, SC
 
dc.contributor.authorLan, F
 
dc.contributor.authorPoon, RTP
 
dc.contributor.authorWadhwa, R
 
dc.contributor.authorLuk, JM
 
dc.date.accessioned2011-07-27T01:37:01Z
 
dc.date.available2011-07-27T01:37:01Z
 
dc.date.issued2011
 
dc.description.abstractStress protein mortalin (mtHSP70) is highly expressed in cancer cells. It was shown to contribute to carcinogenesis by sequestrating the wild type p53, a key tumor suppressor protein, in the cytoplasm resulting in an abrogation of its transcriptional activation function. We have found that the level of mortalin expression has significant correlation with human hepatocellular carcinoma (HCC) malignancy and therefore investigated whether it interacts with and influences the activities of mutant p53, frequently associated with HCC development. We have detected mortalin-p53 interactions in liver tumor and five HCC cell lines that harbored mutant p53. The data was in contrast to the normal liver and immortalized normal hepatocytes that lacked mortalin-p53 interaction. Furthermore, we have found that the shRNA-mediated mortalin silencing could induce mutant p53-mediated tumor-specific apoptosis in HCC. Such allotment of apoptotic function to mutant p53 by targeting mortalin-p53 interaction in cancer cells is a promising strategy for HCC therapy. Copyright © 2010 UICC.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationInternational Journal Of Cancer, 2011, v. 129 n. 8, p. 1806-1814 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.25857
 
dc.identifier.doihttp://dx.doi.org/10.1002/ijc.25857
 
dc.identifier.epage1814
 
dc.identifier.hkuros188089
 
dc.identifier.isiWOS:000294224300002
Funding AgencyGrant Number
The HKU CRCG
New Energy & Industrial Technology Development Organization (NEDO)
Funding Information:

Grant sponsors: The HKU CRCG seed fund, New Energy & Industrial Technology Development Organization (NEDO) and Grant-in-Aid for Japan Society for the Promotion of Science (JSPS), Japan

 
dc.identifier.issn0020-7136
2013 Impact Factor: 5.007
 
dc.identifier.issue8
 
dc.identifier.openurl
 
dc.identifier.pmid21165951
 
dc.identifier.scopuseid_2-s2.0-80052036411
 
dc.identifier.spage1806
 
dc.identifier.urihttp://hdl.handle.net/10722/135551
 
dc.identifier.volume129
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
dc.publisher.placeUnited States
 
dc.relation.ispartofInternational Journal of Cancer
 
dc.relation.referencesReferences in Scopus
 
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc..
 
dc.subjecthuman hepatocellular carcinoma
 
dc.subjectmortalin
 
dc.subjectmutant p53-dependent apoptosis
 
dc.subjectRNAi
 
dc.subjecttherapy
 
dc.titleInduction of mutant p53-dependent apoptosis in human hepatocellular carcinoma by targeting stress protein mortalin
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong
  2. Stanford University School of Medicine
  3. National Institute of Advanced Industrial Science and Technology
  4. National University of Singapore