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
2011 Impact Factor: 3.757
2011 SCImago Journal Rankings: 0.442
DOIhttp://dx.doi.org/10.2119/molmed.2011.00008
ReferencesReferences in Scopus
DC Field
Value
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.natureLink_to_subscribed_fulltext
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
2011 Impact Factor: 3.757
2011 SCImago Journal Rankings: 0.442
dc.identifier.issue7-8
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.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
Author Affiliations
  1. Wenzhou Medical College
  2. National Tsing Hua University
  3. Chinese University of Hong Kong