ABI3, a component of the WAVE2 complex, is potentially regulated by PI3K/AKT pathway

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dc.citation.issue40
dc.citation.volume8
dc.contributor.authorMoraes, Lais [UNIFESP]
dc.contributor.authorZanchin, Nilson I. T.
dc.contributor.authorCerutti, Janete M. [UNIFESP]
dc.coverageOrchard Park
dc.date.accessioned2020-08-04T13:40:11Z
dc.date.available2020-08-04T13:40:11Z
dc.date.issued2017
dc.description.abstractWe previously reported that ABI3 expression is lost in follicular thyroid carcinomas and its restoration significantly inhibited cell growth, invasiveness, migration, and reduced tumor growth in vivo. The mechanistic basis by which ABI3 exerts its tumor suppressive effects is not fully understood. In this study, we show that ABI3 is a phosphoprotein. Using proteomic array analysis, we showed that ABI3 modulated distinct cancer-related pathways in thyroid cancer cells. The KEA analysis found that PI3K substrates were enriched and forced expression of ABI3 markedly decreased the phosphorylation of AKT and the downstream-targeted protein pGSK3 beta. We next used immunoprecipitation combined with mass spectrometry to identify ABI3-interacting proteins that may be involved in modulating/integrating signaling pathways. We identified 37 ABI3 partners, including several components of the canonical WAVE regulatory complex (WRC) such as WAVE2/CYF1P1/NAP1, suggesting that ABI3 function might be regulated through WRC. Both, pharmacological inhibition of the PI3K/AKT pathway and mutation at residue S342 of ABI3, which is predicted to be phosphorylated by AKT, provided evidences that the non-phosphorylated form of ABI3 is preferentially present in the WRC protein complex. Collectively, our findings suggest that ABI3 might be a downstream mediator of the PI3K/AKT pathway that might disrupt WRC via ABI3 phosphorylation.en
dc.description.affiliationUniv Fed Sao Paulo, Genet Bases Thyroid Tumors Lab, Div Genet, Dept Morphol & Genet,Escola Paulista Med, Sao Paulo, Brazil
dc.description.affiliationFundacao Oswaldo Cruz, FIOCRUZ, Inst Carlos Chagas, Curitiba, Parana, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Genet Bases Thyroid Tumors Lab, Div Genet, Dept Morphol & Genet,Escola Paulista Med, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipSao Paulo State Research Foundation (FAPESP)
dc.description.sponsorshipIDFAPESP: 2013/03867-5
dc.description.sponsorshipIDFAPESP: 2014/046570-6
dc.format.extent67769-67781
dc.identifierhttps://doi.org/10.18632/oncotarget.18840
dc.identifier.citationOncotarget. Orchard Park, v. 8, n. 40, p. 67769-67781, 2017.
dc.identifier.fileWOS000410790500078.pdf
dc.identifier.issn1949-2553
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/57356
dc.identifier.wosWOS:000410790500078
dc.language.isoeng
dc.publisherImpact Journals Llc
dc.relation.ispartofOncotarget
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectABI3en
dc.subjectfollicular thyroid carcinomaen
dc.subjectWAVE2en
dc.subjectCYFIP1en
dc.subjectPI3K/AKTen
dc.titleABI3, a component of the WAVE2 complex, is potentially regulated by PI3K/AKT pathwayen
dc.typeinfo:eu-repo/semantics/article
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