CXCR7 reactivates ERK signaling to promote resistance to EGFR kinase inhibitors in NSCLC.

Although EGFR mutant-selective TKIs are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical GPCR, activates the MAPK-ERK pathway via β-arrestin. Depletion of CXCR7...

Täydet tiedot

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Bibliografiset tiedot
Julkaisussa:Cancer Res
Päätekijät: Becker, Jeffrey H., Gao, Yandi, Soucheray, Margaret, Pulido, Ines, Kikuchi, Eiki, Rodríguez, María L., Gandhi, Rutu, Lafuente-Sanchis, Aranzazu, Aupí, Miguel, Fernández-Coronado, Javier Alcácer, Martín-Martorell, Paloma, Cremades, Antonio, Galbis-Caravajal, José M., Alcácer, Javier, Christensen, Camilla L., Simms, Patricia, Hess, Ashley, Asahina, Hajime, Kahle, Michael P., Al-Shahrour, Fatima, Borgia, Jeffrey A., Lahoz, Agustín, Insa, Amelia, Juan, Oscar, Jänne, Pasi A., Wong, Kwok-Kin, Carretero, Julian, Shimamura, Takeshi
Aineistotyyppi: Artigo
Kieli:Inglês
Julkaistu: 2019
Aiheet:
Article
Linkit:https://ncbi.nlm.nih.gov/pmc/articles/PMC6746175/
https://ncbi.nlm.nih.gov/pubmed/31273063
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1158/0008-5472.CAN-19-0024
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