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Article: Targeting S100p inhibits colon cancer growth and metastasis by lentivirus-mediated RNA interference and proteomic analysis

TitleTargeting S100p inhibits colon cancer growth and metastasis by lentivirus-mediated RNA interference and proteomic analysis
Authors
Issue Date2011
PublisherThe Feinstein Institute for Medical Research. The Journal's web site is located at http://www.molmed.org
Citation
Molecular Medicine, 2011, v. 17 n. 7-8, p. 709-716 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/168546
ISSN
2015 Impact Factor: 3.53
2015 SCImago Journal Rankings: 2.372
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJiang, Len_US
dc.contributor.authorLai, YKen_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorWang, Hen_US
dc.contributor.authorLin, MCMen_US
dc.contributor.authorHe, MLen_US
dc.contributor.authorKung, HFen_US
dc.date.accessioned2012-10-08T03:20:24Z-
dc.date.available2012-10-08T03:20:24Z-
dc.date.issued2011en_US
dc.identifier.citationMolecular Medicine, 2011, v. 17 n. 7-8, p. 709-716en_US
dc.identifier.issn1076-1551en_US
dc.identifier.urihttp://hdl.handle.net/10722/168546-
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.en_US
dc.languageengen_US
dc.publisherThe Feinstein Institute for Medical Research. The Journal's web site is located at http://www.molmed.orgen_US
dc.relation.ispartofMolecular Medicineen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCalcium-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Movementen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshColonic Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshElectrophoresis, Gel, Two-Dimensionalen_US
dc.subject.meshGuanine Nucleotide Dissociation Inhibitors - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLentivirus - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshNeoplasm Metastasisen_US
dc.subject.meshNeoplasm Proteins - Genetics - Metabolismen_US
dc.subject.meshProteomics - Methodsen_US
dc.subject.meshRna Interferenceen_US
dc.subject.meshSpectrometry, Mass, Matrix-Assisted Laser Desorption-Ionizationen_US
dc.subject.meshThioredoxins - Metabolismen_US
dc.subject.meshTubulin - Metabolismen_US
dc.subject.meshTumor Burden - Geneticsen_US
dc.subject.meshUp-Regulationen_US
dc.subject.meshXenograft Model Antitumor Assaysen_US
dc.titleTargeting S100p inhibits colon cancer growth and metastasis by lentivirus-mediated RNA interference and proteomic analysisen_US
dc.typeArticleen_US
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, MCM=rp00746en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.2119/molmed.2011.00008en_US
dc.identifier.pmid21327297-
dc.identifier.pmcidPMC3146612-
dc.identifier.scopuseid_2-s2.0-79960726340en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79960726340&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume17en_US
dc.identifier.issue7-8en_US
dc.identifier.spage709en_US
dc.identifier.epage716en_US
dc.identifier.isiWOS:000293681600014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridJiang, L=37000894400en_US
dc.identifier.scopusauthoridLai, YK=7401512434en_US
dc.identifier.scopusauthoridZhang, J=17347152100en_US
dc.identifier.scopusauthoridWang, H=7501747965en_US
dc.identifier.scopusauthoridLin, MCM=7404816359en_US
dc.identifier.scopusauthoridHe, ML=35080389700en_US
dc.identifier.scopusauthoridKung, HF=7402514190en_US

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