Publication: 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.author | Lobos-González, Lorena | |
dc.contributor.author | Oróstica, Lorena | |
dc.contributor.author | Díaz, Natalia | |
dc.contributor.author | Rojas, Victoria | |
dc.contributor.author | Campos, America | |
dc.contributor.author | Duran, Eduardo | |
dc.contributor.author | Farfán, Nicole | |
dc.contributor.author | Farfán, Nicole | |
dc.contributor.author | Leyton, Lisette | |
dc.contributor.author | Quest, Andrew | |
dc.date.accessioned | 2024-05-30T19:32:28Z | |
dc.date.available | 2024-05-30T19:32:28Z | |
dc.date.issued | 2023 | |
dc.description.abstract | Caveolin-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. | |
dc.description.version | Publicada | |
dc.identifier.citation | Lobos-González L, Oróstica L, Díaz-Valdivia N, Rojas-Celis V, Campos A, Duran-Jara E, Farfán N, Leyton L, Quest AFG. Prostaglandin E2 Exposure Disrupts E-Cadherin/Caveolin-1-Mediated Tumor Suppression to Favor Caveolin-1-Enhanced Migration, Invasion, and Metastasis in Melanoma Models. Int J Mol Sci. 2023 Nov 29;24(23):16947. doi: 10.3390/ijms242316947 | |
dc.identifier.doi | https://doi.org/10.3390/ijms242316947 | |
dc.identifier.uri | https://hdl.handle.net/11447/8966 | |
dc.language.iso | en | |
dc.subject | Caveolin-1 | |
dc.subject | E-cadherin | |
dc.subject | PGE2 | |
dc.subject | inflammation | |
dc.subject | tumor progression | |
dc.title | Prostaglandin E2 Exposure Disrupts E-Cadherin/Caveolin-1-Mediated Tumor Suppression to Favor Caveolin-1-Enhanced Migration, Invasion, and Metastasis in Melanoma Models | |
dc.type | Article | |
dcterms.accessRights | Acceso Abierto | |
dcterms.source | International journal of molecular sciences | |
dspace.entity.type | Publication |
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