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Article: Targeting S100p inhibits colon cancer growth and metastasis by lentivirus-mediated RNA interference and proteomic analysis
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TitleTargeting S100p inhibits colon cancer growth and metastasis by lentivirus-mediated RNA interference and proteomic analysis
 
AuthorsJiang, L1
Lai, YK2
Zhang, J3
Wang, H3
Lin, MCM3
He, ML3
Kung, HF3
 
Issue Date2011
 
PublisherThe Feinstein Institute for Medical Research. The Journal's web site is located at http://www.molmed.org
 
CitationMolecular Medicine, 2011, v. 17 n. 7-8, p. 709-716 [How to Cite?]
DOI: http://dx.doi.org/10.2119/molmed.2011.00008
 
AbstractS100P was recently found to be overexpressed in a variety of cancers and is considered a potential target for cancer therapy, but the functional role or mechanism of action of S100P in colon cancer is not fully understood. In the present study, we knocked down the gene expression of S100P in colon cancer cells using lentivirus-mediated RNA interference. This step resulted in significant inhibition of cancer cell growth, migration and invasion in vitro and tumor growth and liver metastasis in vivo. Moreover, S100P downstream target proteins were identified by proteomic analysis in colon cancer DLD-1 cells with deletion of S100P. Knockdown of S100P led to downregulation of thioredoxin 1 and β-tubulin and upregulation of Rho guanosine diphosphate (GDP) dissociation inhibitor α (RhoGDIA), all potential therapeutic targets in cancer. Taken together, these findings suggest that S100P plays an important role in colon tumorigenesis and metastasis, and the comprehensive and comparative analyses of proteins associated with S100P could contribute to understanding the downstream signal cascade of S100P, leading to tumorigenesis and metastasis. © 2011 The Feinstein Institute for Medical Research.
 
ISSN1076-1551
2013 Impact Factor: 4.824
 
DOIhttp://dx.doi.org/10.2119/molmed.2011.00008
 
PubMed Central IDPMC3146612
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorJiang, L
 
dc.contributor.authorLai, YK
 
dc.contributor.authorZhang, J
 
dc.contributor.authorWang, H
 
dc.contributor.authorLin, MCM
 
dc.contributor.authorHe, ML
 
dc.contributor.authorKung, HF
 
dc.date.accessioned2012-10-08T03:20:24Z
 
dc.date.available2012-10-08T03:20:24Z
 
dc.date.issued2011
 
dc.description.abstractS100P was recently found to be overexpressed in a variety of cancers and is considered a potential target for cancer therapy, but the functional role or mechanism of action of S100P in colon cancer is not fully understood. In the present study, we knocked down the gene expression of S100P in colon cancer cells using lentivirus-mediated RNA interference. This step resulted in significant inhibition of cancer cell growth, migration and invasion in vitro and tumor growth and liver metastasis in vivo. Moreover, S100P downstream target proteins were identified by proteomic analysis in colon cancer DLD-1 cells with deletion of S100P. Knockdown of S100P led to downregulation of thioredoxin 1 and β-tubulin and upregulation of Rho guanosine diphosphate (GDP) dissociation inhibitor α (RhoGDIA), all potential therapeutic targets in cancer. Taken together, these findings suggest that S100P plays an important role in colon tumorigenesis and metastasis, and the comprehensive and comparative analyses of proteins associated with S100P could contribute to understanding the downstream signal cascade of S100P, leading to tumorigenesis and metastasis. © 2011 The Feinstein Institute for Medical Research.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationMolecular Medicine, 2011, v. 17 n. 7-8, p. 709-716 [How to Cite?]
DOI: http://dx.doi.org/10.2119/molmed.2011.00008
 
dc.identifier.doihttp://dx.doi.org/10.2119/molmed.2011.00008
 
dc.identifier.epage716
 
dc.identifier.issn1076-1551
2013 Impact Factor: 4.824
 
dc.identifier.issue7-8
 
dc.identifier.pmcidPMC3146612
 
dc.identifier.pmid21327297
 
dc.identifier.scopuseid_2-s2.0-79960726340
 
dc.identifier.spage709
 
dc.identifier.urihttp://hdl.handle.net/10722/168546
 
dc.identifier.volume17
 
dc.languageeng
 
dc.publisherThe Feinstein Institute for Medical Research. The Journal's web site is located at http://www.molmed.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofMolecular Medicine
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshAnimals
 
dc.subject.meshBlotting, Western
 
dc.subject.meshCalcium-Binding Proteins - Genetics - Metabolism
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshCell Movement
 
dc.subject.meshCell Proliferation
 
dc.subject.meshColonic Neoplasms - Genetics - Metabolism - Pathology
 
dc.subject.meshDown-Regulation
 
dc.subject.meshElectrophoresis, Gel, Two-Dimensional
 
dc.subject.meshGuanine Nucleotide Dissociation Inhibitors - Metabolism
 
dc.subject.meshHumans
 
dc.subject.meshLentivirus - Genetics
 
dc.subject.meshMale
 
dc.subject.meshMice
 
dc.subject.meshMice, Nude
 
dc.subject.meshNeoplasm Metastasis
 
dc.subject.meshNeoplasm Proteins - Genetics - Metabolism
 
dc.subject.meshProteomics - Methods
 
dc.subject.meshRna Interference
 
dc.subject.meshSpectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
 
dc.subject.meshThioredoxins - Metabolism
 
dc.subject.meshTubulin - Metabolism
 
dc.subject.meshTumor Burden - Genetics
 
dc.subject.meshUp-Regulation
 
dc.subject.meshXenograft Model Antitumor Assays
 
dc.titleTargeting S100p inhibits colon cancer growth and metastasis by lentivirus-mediated RNA interference and proteomic analysis
 
dc.typeArticle
 
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Author Affiliations
  1. Wenzhou Medical College
  2. National Tsing Hua University
  3. Chinese University of Hong Kong