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Article: MiR-130b promotes CD133 + liver tumor-initiating cell growth and self-renewal via tumor protein 53-induced nuclear protein 1

TitleMiR-130b promotes CD133 + liver tumor-initiating cell growth and self-renewal via tumor protein 53-induced nuclear protein 1
Authors
Issue Date2010
PublisherCell Press. The Journal's web site is located at http://www.cellstemcell.com
Citation
Cell Stem Cell, 2010, v. 7 n. 6, p. 694-707 How to Cite?
AbstractA novel paradigm in tumor biology suggests that cancer growth is driven by stem-like cells within a tumor, called tumor-initiating cells (TICs) or cancer stem cells (CSCs). Here we describe the identification and characterization of such cells from hepatocellular carcinoma (HCC) using the marker CD133. CD133 accounts for approximately 1.3%-13.6% of the cells in the bulk tumor of human primary HCC samples. When compared with their CD133 - counterparts, CD133 + cells not only possess the preferential ability to form undifferentiated tumor spheroids in vitro but also express an enhanced level of stem cell-associated genes, have a greater ability to form tumors when implanted orthotopically in immunodeficient mice, and can be serially passaged into secondary animal recipients. Xenografts resemble the original human tumor and maintain a similar percentage of tumorigenic CD133 + cells. Quantitative PCR analysis of 41 separate HCC tissue specimens with follow-up data found that CD133 + tumor cells were frequently detected at low quantities in HCC, and their presence was also associated with worse overall survival and higher recurrence rates. Subsequent differential microRNA expression profiling of CD133 + and CD133 - cells from human HCC clinical specimens and cell lines identified an overexpression of miR-130b in CD133 + TICs. Functional studies on miR-130b lentiviral-transduced CD133 - cells demonstrated superior resistance to chemotherapeutic agents, enhanced tumorigenicity in vivo, and a greater potential for self renewal. Conversely, antagonizing miR-130b in CD133 + TICs yielded an opposing effect. The increased miR-130b paralleled the reduced TP53INP1, a known miR-130b target. Silencing TP53INP1 in CD133 - cells enhanced both self renewal and tumorigenicity in vivo. Collectively, miR-130b regulates CD133 + liver TICs, in part, via silencing TP53INP1. © 2010 Elsevier Inc.
DescriptionComment in Cell Cycle. 2011 Feb 15;10(4):571-572.
Persistent Identifierhttp://hdl.handle.net/10722/142518
ISSN
2015 Impact Factor: 22.387
2015 SCImago Journal Rankings: 13.121
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council Collaborative Research FundHKU 1/06C
HKU 7/CRG/09
HKU5/CRF/08
National Key Sci-Tech Special Project of Infectious Diseases2008ZX1002-022
University of Hong Kong Strategic Research Theme in Cancer
University of Hong Kong
Funding Information:

The authors would like to thank Dr. Alice Carrier (INSERM; France) for her gift of the monoclonal rat anti-human TP53INP1 (E12) antibody, Drs. Man Lung Yeung and Kuan-The Jeang (NIH; USA) for their gift of the full-length 3'UTR TP53INP1 plasmid, Mr. Fai Ng (University of Hong Kong, HK) for his expert assistance with the cell-sorting facility and Professor George Tsao (Centre for Cancer Research, University of Hong Kong, HK) for his support on cancer stem cell studies. This work was generously supported by Sir Michael and Lady Kadoorie Funded Research into Cancer Genetics, Research Grant Council Collaborative Research Fund (HKU 1/06C, HKU 7/CRG/09 and HKU5/CRF/08), National Key Sci-Tech Special Project of Infectious Diseases (2008ZX1002-022), The University of Hong Kong Strategic Research Theme in Cancer, The University of Hong Kong Seed Funding Program, The University of Hong Kong Small Project Funding Program, and Donation of the Li Ka Shing Foundation of Matching Grants of The University of Hong Kong.

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DC FieldValueLanguage
dc.contributor.authorMa, Sen_HK
dc.contributor.authorTang, KHen_HK
dc.contributor.authorChan, YPen_HK
dc.contributor.authorLee, TKen_HK
dc.contributor.authorKwan, PSen_HK
dc.contributor.authorCastilho, Aen_HK
dc.contributor.authorNg, Ien_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorWong, Nen_HK
dc.contributor.authorTo, KFen_HK
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorLai, PBSen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2011-10-28T02:50:19Z-
dc.date.available2011-10-28T02:50:19Z-
dc.date.issued2010en_HK
dc.identifier.citationCell Stem Cell, 2010, v. 7 n. 6, p. 694-707en_HK
dc.identifier.issn1934-5909en_HK
dc.identifier.urihttp://hdl.handle.net/10722/142518-
dc.descriptionComment in Cell Cycle. 2011 Feb 15;10(4):571-572.-
dc.description.abstractA novel paradigm in tumor biology suggests that cancer growth is driven by stem-like cells within a tumor, called tumor-initiating cells (TICs) or cancer stem cells (CSCs). Here we describe the identification and characterization of such cells from hepatocellular carcinoma (HCC) using the marker CD133. CD133 accounts for approximately 1.3%-13.6% of the cells in the bulk tumor of human primary HCC samples. When compared with their CD133 - counterparts, CD133 + cells not only possess the preferential ability to form undifferentiated tumor spheroids in vitro but also express an enhanced level of stem cell-associated genes, have a greater ability to form tumors when implanted orthotopically in immunodeficient mice, and can be serially passaged into secondary animal recipients. Xenografts resemble the original human tumor and maintain a similar percentage of tumorigenic CD133 + cells. Quantitative PCR analysis of 41 separate HCC tissue specimens with follow-up data found that CD133 + tumor cells were frequently detected at low quantities in HCC, and their presence was also associated with worse overall survival and higher recurrence rates. Subsequent differential microRNA expression profiling of CD133 + and CD133 - cells from human HCC clinical specimens and cell lines identified an overexpression of miR-130b in CD133 + TICs. Functional studies on miR-130b lentiviral-transduced CD133 - cells demonstrated superior resistance to chemotherapeutic agents, enhanced tumorigenicity in vivo, and a greater potential for self renewal. Conversely, antagonizing miR-130b in CD133 + TICs yielded an opposing effect. The increased miR-130b paralleled the reduced TP53INP1, a known miR-130b target. Silencing TP53INP1 in CD133 - cells enhanced both self renewal and tumorigenicity in vivo. Collectively, miR-130b regulates CD133 + liver TICs, in part, via silencing TP53INP1. © 2010 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.subject.meshAntigens, CD - genetics - metabolism-
dc.subject.meshCarcinoma, Hepatocellular - genetics - metabolism-
dc.subject.meshCarrier Proteins - metabolism-
dc.subject.meshGlycoproteins - genetics - metabolism-
dc.subject.meshLiver Neoplasms - genetics - metabolism-
dc.titleMiR-130b promotes CD133 + liver tumor-initiating cell growth and self-renewal via tumor protein 53-induced nuclear protein 1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1934-5909&volume=7&issue=6&spage=694&epage=707&date=2010&atitle=miR-130b+promotes+CD133++liver+tumor-initiating+cell+growth+and+self-renewal+via+tumor+protein+53-induced+nuclear+protein+1-
dc.identifier.emailMa, S: sma@pathology.hku.hken_HK
dc.identifier.emailLee, TK: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailNg, I: iolng@hkucc.hku.hken_HK
dc.identifier.emailMan, K: kwanman@hkucc.hku.hken_HK
dc.identifier.emailZheng, BJ: bzheng@hkucc.hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.authorityMa, S=rp00506en_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityNg, I=rp00335en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.stem.2010.11.010en_HK
dc.identifier.pmid21112564-
dc.identifier.scopuseid_2-s2.0-78649681554en_HK
dc.identifier.hkuros184057en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78649681554&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue6en_HK
dc.identifier.spage694en_HK
dc.identifier.epage707en_HK
dc.identifier.isiWOS:000285537700011-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectMolecular pathology of liver cancer - a multidisciplinary study-
dc.relation.projectLiver Transplantation Research Centre: A Multidisciplinary Study for Liver Graft Injury-
dc.identifier.scopusauthoridMa, S=16444895800en_HK
dc.identifier.scopusauthoridTang, KH=24781597200en_HK
dc.identifier.scopusauthoridChan, YP=14009821700en_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridKwan, PS=36698058700en_HK
dc.identifier.scopusauthoridCastilho, A=35067775500en_HK
dc.identifier.scopusauthoridNg, I=7102753722en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridWong, N=7202836653en_HK
dc.identifier.scopusauthoridTo, KF=7101911940en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridLai, PBS=7202946421en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.citeulike8411888-

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