Prostaglandin E2 Exposure Disrupts E-Cadherin/Caveolin-1-Mediated Tumor Suppression to Favor Caveolin-1-Enhanced Migration, Invasion, and Metastasis in Melanoma Models

dc.contributor.authorLobos-González, Lorena
dc.contributor.authorOróstica, Lorena
dc.contributor.authorDíaz-Valdivia, Natalia
dc.contributor.authorRojas-Celis, Victoria
dc.contributor.authorCampos, America
dc.contributor.authorDuran-Jara, Eduardo
dc.contributor.authorFarfán, Nicole
dc.contributor.authorLeyton, Lisette
dc.contributor.authorQuest, Andrew F. G.
dc.date.accessioned2024-01-02T18:44:53Z
dc.date.available2024-01-02T18:44:53Z
dc.date.issued2023-12
dc.descriptionIndexación: Scopus.es
dc.description.abstractCaveolin-1 (CAV1) is a membrane-bound protein that suppresses tumor development yet also promotes metastasis. E-cadherin is important in CAV1-dependent tumor suppression and prevents CAV1-enhanced lung metastasis. Here, we used murine B16F10 and human A375 melanoma cells with low levels of endogenous CAV1 and E-cadherin to unravel how co-expression of E-cadherin modulates CAV1 function in vitro and in vivo in WT C57BL/6 or Rag−/− immunodeficient mice and how a pro-inflammatory environment generated by treating cells with prostaglandin E2 (PGE2) alters CAV1 function in the presence of E-cadherin. CAV1 expression augmented migration, invasion, and metastasis of melanoma cells, and these effects were abolished via transient co-expression of E-cadherin. Importantly, exposure of cells to PGE2 reverted the effects of E-cadherin expression and increased CAV1 phosphorylation on tyrosine-14 and metastasis. Moreover, PGE2 administration blocked the ability of the CAV1/E-cadherin complex to prevent tumor formation. Therefore, our results support the notion that PGE2 can override the tumor suppressor potential of the E-cadherin/CAV1 complex and that CAV1 released from the complex is phosphorylated on tyrosine-14 and promotes migration/invasion/metastasis. These observations provide direct evidence showing how a pro-inflammatory environment caused here via PGE2 administration can convert a potent tumor suppressor complex into a promoter of malignant cell behavior.es
dc.description.urihttps://www-scopus-com.recursosbiblioteca.unab.cl/record/display.uri?eid=2-s2.0-85179340342&origin=resultslist&sort=plf-f&src=s&sid=2f4a169609be0f23a959b073bcb5745e&sot=aff&sdt=aff&sl=61&s=AF-ID%28%22Universidad+Andr%c3%a9s+Bello%22+60002636%29+AND+SUBJAREA%28CENG%29&relpos=1&citeCnt=0&searchTerm=
dc.identifier.citationInternational Journal of Molecular Sciences, Open Access, Volume 24, Issue 23 December 2023, Article number 16947es
dc.identifier.doi10.3390/ijms242316947
dc.identifier.issn16616596
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/54567
dc.language.isoenes
dc.publisherMDPIes
dc.rights.licenseCC BY 4.0 DEED Attribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectCaveolin-1es
dc.subjectE-cadherines
dc.subjectInflammationes
dc.subjectPGE2es
dc.subjectTumor progressiones
dc.titleProstaglandin E2 Exposure Disrupts E-Cadherin/Caveolin-1-Mediated Tumor Suppression to Favor Caveolin-1-Enhanced Migration, Invasion, and Metastasis in Melanoma Modelses
dc.typeArtículoes
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