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Article: Recognition of CD146 as an ERM-binding protein offers novel mechanisms for melanoma cell migration

TitleRecognition of CD146 as an ERM-binding protein offers novel mechanisms for melanoma cell migration
Authors
KeywordsCD146
RhoA
ERM proteins
cell migration
RhoGDI1
Issue Date2012
Citation
Oncogene, 2012, v. 31, n. 3, p. 306-321 How to Cite?
AbstractTumor cell migration is a well-orchestrated multistep process that drives cancer development and metastasis. Previous data indicated that CD146 expression correlates with malignant progression and metastatic potential of human melanoma cells. However, the exact molecular mechanism of how CD146 promotes melanoma cell migration still remains poorly understood. Here, we report that CD146 physically interacts with actin-linking ezrin-radixin-moesin (ERM) proteins and recruits ERM proteins to cell protrusions, promoting the formation and elongation of microvilli. Moreover, CD146-promoted melanoma cell migration is linked to RhoA activation and ERM phosphorylation. CD146 recruits Rho guanine nucleotide dissociation inhibitory factors 1 (RhoGDI1) through ERM proteins and thus sequesters RhoGDI1 from RhoA, which leads to upregulated RhoA activity and increased melanoma cell motility. CD146-activated RhoA also promotes further ERM phosphorylation and activation through Rho-phosphatidylinositol-4-phosphate- 5-kinase-phosphatidylinositol 4,5-biphosphate pathway, which reinforces CD146/ERM association. Thus, our results provide a mechanistic basis to understand the role of CD146 in regulating human melanoma cell motility. © 2012 Macmillan Publishers Limited All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/265472
ISSN
2019 Impact Factor: 7.971
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLuo, Y.-
dc.contributor.authorZheng, C.-
dc.contributor.authorZhang, J.-
dc.contributor.authorLu, D.-
dc.contributor.authorZhuang, J.-
dc.contributor.authorXing, S.-
dc.contributor.authorFeng, J.-
dc.contributor.authorYang, D.-
dc.contributor.authorYan, X.-
dc.date.accessioned2018-12-03T01:20:46Z-
dc.date.available2018-12-03T01:20:46Z-
dc.date.issued2012-
dc.identifier.citationOncogene, 2012, v. 31, n. 3, p. 306-321-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://hdl.handle.net/10722/265472-
dc.description.abstractTumor cell migration is a well-orchestrated multistep process that drives cancer development and metastasis. Previous data indicated that CD146 expression correlates with malignant progression and metastatic potential of human melanoma cells. However, the exact molecular mechanism of how CD146 promotes melanoma cell migration still remains poorly understood. Here, we report that CD146 physically interacts with actin-linking ezrin-radixin-moesin (ERM) proteins and recruits ERM proteins to cell protrusions, promoting the formation and elongation of microvilli. Moreover, CD146-promoted melanoma cell migration is linked to RhoA activation and ERM phosphorylation. CD146 recruits Rho guanine nucleotide dissociation inhibitory factors 1 (RhoGDI1) through ERM proteins and thus sequesters RhoGDI1 from RhoA, which leads to upregulated RhoA activity and increased melanoma cell motility. CD146-activated RhoA also promotes further ERM phosphorylation and activation through Rho-phosphatidylinositol-4-phosphate- 5-kinase-phosphatidylinositol 4,5-biphosphate pathway, which reinforces CD146/ERM association. Thus, our results provide a mechanistic basis to understand the role of CD146 in regulating human melanoma cell motility. © 2012 Macmillan Publishers Limited All rights reserved.-
dc.languageeng-
dc.relation.ispartofOncogene-
dc.subjectCD146-
dc.subjectRhoA-
dc.subjectERM proteins-
dc.subjectcell migration-
dc.subjectRhoGDI1-
dc.titleRecognition of CD146 as an ERM-binding protein offers novel mechanisms for melanoma cell migration-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/onc.2011.244-
dc.identifier.pmid21725352-
dc.identifier.scopuseid_2-s2.0-84855946358-
dc.identifier.volume31-
dc.identifier.issue3-
dc.identifier.spage306-
dc.identifier.epage321-
dc.identifier.eissn1476-5594-
dc.identifier.isiWOS:000299542100004-
dc.identifier.issnl0950-9232-

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