Proteomics-based strategy to delineate the molecular mechanisms of RhoGDI2-induced metastasis and drug resistance in gastric cancer

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dc.contributor.authorHee Jun Cho-
dc.contributor.authorK E Baek-
dc.contributor.authorI K Kim-
dc.contributor.authorS M Park-
dc.contributor.authorY L Choi-
dc.contributor.authorI K Nam-
dc.contributor.authorS H Park-
dc.contributor.authorM J Im-
dc.contributor.authorJ M Yoo-
dc.contributor.authorK J Ryu-
dc.contributor.authorY T Oh-
dc.contributor.authorS C Hong-
dc.contributor.authorOh Hyung Kwon-
dc.contributor.authorJ W Kim-
dc.contributor.authorC W Lee-
dc.contributor.authorJ Yoo-
dc.date.accessioned2017-04-19T09:29:40Z-
dc.date.available2017-04-19T09:29:40Z-
dc.date.issued2012-
dc.identifier.issn1535-3893-
dc.identifier.uri10.1021/pr2011186ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/10688-
dc.description.abstractRho GDP dissociation inhibitor 2 (RhoGDI2) was initially identified as a regulator of the Rho family of GTPases. Our recent works suggest that RhoGDI2 promotes tumor growth and malignant progression, as well as enhances chemoresistance in gastric cancer. Here, we delineate the mechanism by which RhoGDI2 promotes gastric cancer cell invasion and chemoresistance using two-dimensional gel electrophoresis (2-DE) on proteins derived from a RhoGDI2-overexpressing SNU-484 human gastric cancer cell line and control cells. Differentially expressed proteins were identified using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry (MALDI-TOF-MS). In total, 47 differential protein spots were identified; 33 were upregulated, and 14 were downregulated by RhoGDI2 overexpression. Upregulation of SAE1, Cathepsin D, Cofilin1, CIAPIN1, and PAK2 proteins was validated by Western blot analysis. Loss-of-function analysis using small interference RNA (siRNA) directed against candidate genes reveals the need for CIAPIN1 and PAK2 in RhoGDI2-induced cancer cell invasion and Cathepsin D and PAK2 in RhoGDI2-mediated chemoresistance in gastric cancer cells. These data extend our understanding of the genes that act downstream of RhoGDI2 during the progression of gastric cancer and the acquisition of chemoresistance.-
dc.publisherAmer Chem Soc-
dc.titleProteomics-based strategy to delineate the molecular mechanisms of RhoGDI2-induced metastasis and drug resistance in gastric cancer-
dc.title.alternativeProteomics-based strategy to delineate the molecular mechanisms of RhoGDI2-induced metastasis and drug resistance in gastric cancer-
dc.typeArticle-
dc.citation.titleJournal of Proteome Research-
dc.citation.number4-
dc.citation.endPage2364-
dc.citation.startPage2355-
dc.citation.volume11-
dc.contributor.affiliatedAuthorHee Jun Cho-
dc.contributor.affiliatedAuthorOh Hyung Kwon-
dc.contributor.alternativeName조희준-
dc.contributor.alternativeName백경은-
dc.contributor.alternativeName김인규-
dc.contributor.alternativeName박선미-
dc.contributor.alternativeName최영림-
dc.contributor.alternativeName남인구-
dc.contributor.alternativeName박승호-
dc.contributor.alternativeName임민주-
dc.contributor.alternativeName유종민-
dc.contributor.alternativeName류기준-
dc.contributor.alternativeName오영택-
dc.contributor.alternativeName홍순찬-
dc.contributor.alternativeName권오형-
dc.contributor.alternativeName김재원-
dc.contributor.alternativeName이창원-
dc.contributor.alternativeName유지연-
dc.identifier.bibliographicCitationJournal of Proteome Research, vol. 11, no. 4, pp. 2355-2364-
dc.identifier.doi10.1021/pr2011186-
dc.subject.keywordcathepsin D-
dc.subject.keywordCIAPIN1-
dc.subject.keywordcisplatin resistance-
dc.subject.keywordgastric cancer-
dc.subject.keywordinvasion-
dc.subject.keywordmetastasis-
dc.subject.keywordPAK2-
dc.subject.keywordRhoGDI2-
dc.subject.localcathepsin D-
dc.subject.localCIAPIN1-
dc.subject.localcisplatin resistance-
dc.subject.localCisplatin resistance-
dc.subject.localgastric cancer-
dc.subject.localGastric cancer (GC)-
dc.subject.localGastric cancer-
dc.subject.localinvasion-
dc.subject.localInvasion-
dc.subject.localmetastasis-
dc.subject.localMetastasis-
dc.subject.localPAK2-
dc.subject.localRhoGDI2-
dc.description.journalClassY-
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Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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