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Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition.

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dc.contributor.authorMateo, F
dc.contributor.authorArenas, E J
dc.contributor.authorAguilar, H
dc.contributor.authorSerra-Musach, J
dc.contributor.authorde Garibay, G Ruiz
dc.contributor.authorBoni, J
dc.contributor.authorMaicas, M
dc.contributor.authorDu, S
dc.contributor.authorIorio, F
dc.contributor.authorHerranz-Ors, C
dc.contributor.authorIslam, A
dc.contributor.authorPrado, X
dc.contributor.authorLlorente, A
dc.contributor.authorPetit, A
dc.contributor.authorVidal, A
dc.contributor.authorCatalà, I
dc.contributor.authorSoler, T
dc.contributor.authorVenturas, G
dc.contributor.authorRojo-Sebastian, A
dc.contributor.authorSerra, H
dc.contributor.authorCuadras, D
dc.contributor.authorBlanco, I
dc.contributor.authorLozano, J
dc.contributor.authorCanals, F
dc.contributor.authorSieuwerts, A M
dc.contributor.authorde Weerd, V
dc.contributor.authorLook, M P
dc.contributor.authorPuertas, S
dc.contributor.authorGarcía, N
dc.contributor.authorPerkins, A S
dc.contributor.authorBonifaci, N
dc.contributor.authorSkowron, M
dc.contributor.authorGómez-Baldó, L
dc.contributor.authorHernández, V
dc.contributor.authorMartínez-Aranda, A
dc.contributor.authorMartínez-Iniesta, M
dc.contributor.authorSerrat, X
dc.contributor.authorCerón, J
dc.contributor.authorBrunet, J
dc.contributor.authorBarretina, M P
dc.contributor.authorGil, M
dc.contributor.authorFalo, C
dc.contributor.authorFernández, A
dc.contributor.authorMorilla, I
dc.contributor.authorPernas, S
dc.contributor.authorPlà, M J
dc.contributor.authorAndreu, X
dc.contributor.authorSeguí, M A
dc.contributor.authorBallester, R
dc.contributor.authorCastellà, E
dc.contributor.authorNellist, M
dc.contributor.authorMorales, S
dc.contributor.authorValls, J
dc.contributor.authorVelasco, A
dc.contributor.authorMatias-Guiu, X
dc.contributor.authorFigueras, A
dc.contributor.authorSánchez-Mut, J V
dc.contributor.authorSánchez-Céspedes, M
dc.contributor.authorCordero, A
dc.contributor.authorGómez-Miragaya, J
dc.contributor.authorPalomero, L
dc.contributor.authorGómez, A
dc.contributor.authorGajewski, T F
dc.contributor.authorCohen, E E W
dc.contributor.authorJesiotr, M
dc.contributor.authorBodnar, L
dc.contributor.authorQuintela-Fandino, M
dc.contributor.authorLópez-Bigas, N
dc.contributor.authorValdés-Mas, R
dc.contributor.authorPuente, X S
dc.contributor.authorViñals, F
dc.contributor.authorCasanovas, O
dc.contributor.authorGraupera, M
dc.contributor.authorHernández-Losa, J
dc.contributor.authorRamón Y Cajal, S
dc.contributor.authorGarcía-Alonso, L
dc.contributor.authorSaez-Rodriguez, J
dc.contributor.authorEsteller, M
dc.contributor.authorSierra, A
dc.contributor.authorMartín-Martín, N
dc.contributor.authorMatheu, A
dc.contributor.authorCarracedo, A
dc.contributor.authorGonzález-Suárez, E
dc.contributor.authorNanjundan, M
dc.contributor.authorCortés, J
dc.contributor.authorLázaro, C
dc.contributor.authorOdero, M D
dc.contributor.authorMartens, J W M
dc.contributor.authorMoreno-Bueno, G
dc.contributor.authorBarcellos-Hoff, M H
dc.contributor.authorVillanueva, A
dc.contributor.authorGomis, R R
dc.contributor.authorPujana, M A
dc.date.accessioned2023-01-25T09:42:40Z
dc.date.available2023-01-25T09:42:40Z
dc.date.issued2016-12-19
dc.description.abstractInhibitors of the mechanistic target of rapamycin (mTOR) are currently used to treat advanced metastatic breast cancer. However, whether an aggressive phenotype is sustained through adaptation or resistance to mTOR inhibition remains unknown. Here, complementary studies in human tumors, cancer models and cell lines reveal transcriptional reprogramming that supports metastasis in response to mTOR inhibition. This cancer feature is driven by EVI1 and SOX9. EVI1 functionally cooperates with and positively regulates SOX9, and promotes the transcriptional upregulation of key mTOR pathway components (REHB and RAPTOR) and of lung metastasis mediators (FSCN1 and SPARC). The expression of EVI1 and SOX9 is associated with stem cell-like and metastasis signatures, and their depletion impairs the metastatic potential of breast cancer cells. These results establish the mechanistic link between resistance to mTOR inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR targeting failure.
dc.identifier.doi10.1038/onc.2016.427
dc.identifier.essn1476-5594
dc.identifier.pmcPMC5442428
dc.identifier.pmid27991928
dc.identifier.pubmedURLhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442428/pdf
dc.identifier.unpaywallURLhttps://www.nature.com/articles/onc2016427.pdf
dc.identifier.urihttp://hdl.handle.net/10668/10692
dc.issue.number19
dc.journal.titleOncogene
dc.journal.titleabbreviationOncogene
dc.language.isoen
dc.organizationHospital Universitario Virgen de la Victoria
dc.page.number2737-2749
dc.pubmedtypeJournal Article
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.meshAdaptor Proteins, Signal Transducing
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshBreast Neoplasms
dc.subject.meshCarrier Proteins
dc.subject.meshCell Proliferation
dc.subject.meshDNA-Binding Proteins
dc.subject.meshFemale
dc.subject.meshGene Expression Regulation, Neoplastic
dc.subject.meshHumans
dc.subject.meshLung Neoplasms
dc.subject.meshMCF-7 Cells
dc.subject.meshMDS1 and EVI1 Complex Locus Protein
dc.subject.meshMicrofilament Proteins
dc.subject.meshMiddle Aged
dc.subject.meshNeoplasm Metastasis
dc.subject.meshOsteonectin
dc.subject.meshProto-Oncogenes
dc.subject.meshRegulatory-Associated Protein of mTOR
dc.subject.meshSOX9 Transcription Factor
dc.subject.meshSignal Transduction
dc.subject.meshTOR Serine-Threonine Kinases
dc.subject.meshTranscription Factors
dc.subject.meshXenograft Model Antitumor Assays
dc.titleStem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number36
dspace.entity.typePublication

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