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Article: CD24 + Liver Tumor-Initiating Cells Drive Self-Renewal and Tumor Initiation through STAT3-Mediated NANOG Regulation

TitleCD24 + Liver Tumor-Initiating Cells Drive Self-Renewal and Tumor Initiation through STAT3-Mediated NANOG Regulation
Authors
KeywordsCD24 antigen
Cisplatin
STAT3 protein
Cell differentiation
Cell renewal
Issue Date2011
PublisherCell Press. The Journal's web site is located at http://www.cellstemcell.com
Citation
Cell Stem Cell, 2011, v. 9 n. 1, p. 50-63 How to Cite?
AbstractTumor-initiating cells (T-ICs) are a subpopulation of chemoresistant tumor cells that have been shown to cause tumor recurrence upon chemotherapy. Identification of T-ICs and their related pathways are therefore priorities for the development of new therapeutic paradigms. We established chemoresistant hepatocellular carcinoma (HCC) xenograft tumors in immunocompromised mice in which an enriched T-IC population was capable of tumor initiation and self-renewal. With this model, we found CD24 to be upregulated in residual chemoresistant tumors when compared with bulk tumor upon cisplatin treatment. CD24 + HCC cells were found to be critical for the maintenance, self-renewal, differentiation, and metastasis of tumors and to significantly impact patients' clinical outcome. With a lentiviral-based knockdown approach, CD24 was found to be a functional liver T-IC marker that drives T-IC genesis through STAT3-mediated NANOG regulation. Our findings point to a CD24 cascade in liver T-ICs that may provide an attractive therapeutic target for HCC patients. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/137620
ISSN
2023 Impact Factor: 19.8
2023 SCImago Journal Rankings: 10.253
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants CouncilHKU 1/06C
HKU 7/CRF/09
Funding Information:

The authors would like to thank LKS Faculty of Medicine at The University of Hong Kong for the Faculty Core Facility. The study was supported by Hong Kong Research Grants Council Collaborative Research Fund (HKU 1/06C and HKU 7/CRF/09). I.O.L.N. is Loke Yew Professor in Pathology.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLee, TKWen_HK
dc.contributor.authorCastilho, Aen_HK
dc.contributor.authorCheung, VCHen_HK
dc.contributor.authorTang, KHen_HK
dc.contributor.authorMa, Sen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2011-08-26T14:29:28Z-
dc.date.available2011-08-26T14:29:28Z-
dc.date.issued2011en_HK
dc.identifier.citationCell Stem Cell, 2011, v. 9 n. 1, p. 50-63en_HK
dc.identifier.issn1934-5909en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137620-
dc.description.abstractTumor-initiating cells (T-ICs) are a subpopulation of chemoresistant tumor cells that have been shown to cause tumor recurrence upon chemotherapy. Identification of T-ICs and their related pathways are therefore priorities for the development of new therapeutic paradigms. We established chemoresistant hepatocellular carcinoma (HCC) xenograft tumors in immunocompromised mice in which an enriched T-IC population was capable of tumor initiation and self-renewal. With this model, we found CD24 to be upregulated in residual chemoresistant tumors when compared with bulk tumor upon cisplatin treatment. CD24 + HCC cells were found to be critical for the maintenance, self-renewal, differentiation, and metastasis of tumors and to significantly impact patients' clinical outcome. With a lentiviral-based knockdown approach, CD24 was found to be a functional liver T-IC marker that drives T-IC genesis through STAT3-mediated NANOG regulation. Our findings point to a CD24 cascade in liver T-ICs that may provide an attractive therapeutic target for HCC patients. © 2011 Elsevier Inc.en_HK
dc.languageengen_US
dc.publisherCell Press. The Journal's web site is located at http://www.cellstemcell.comen_HK
dc.relation.ispartofCell Stem Cellen_HK
dc.rights© 2011. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subjectCD24 antigen-
dc.subjectCisplatin-
dc.subjectSTAT3 protein-
dc.subjectCell differentiation-
dc.subjectCell renewal-
dc.titleCD24 + Liver Tumor-Initiating Cells Drive Self-Renewal and Tumor Initiation through STAT3-Mediated NANOG Regulationen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, TKW:tkwlee@hkucc.hku.hken_HK
dc.identifier.emailMa, S:sma@pathology.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.authorityLee, TKW=rp00447en_HK
dc.identifier.authorityMa, S=rp00506en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.stem.2011.06.005en_HK
dc.identifier.pmid21726833-
dc.identifier.scopuseid_2-s2.0-79960006754en_HK
dc.identifier.hkuros189781en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79960006754&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume9en_HK
dc.identifier.issue1en_HK
dc.identifier.spage50en_HK
dc.identifier.epage63en_HK
dc.identifier.eissn1875-9777-
dc.identifier.isiWOS:000293157000009-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectMolecular Pathology of Liver Cancer - a Multidisciplinary Study-
dc.relation.projectMolecular pathology of liver cancer - a multidisciplinary study-
dc.identifier.issnl1875-9777-

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