Cell plasticity-related phenotypes and taxanes resistance in castration-resistant prostate cáncer

The prostatic tumor cells plasticity is involved in resistance to hormone-therapy, allowing these cells to survive despite androgen receptor inhibition. However, its role in taxanes resistance has not been fully established. Gene expression of plasticity-related phenotypes such as epithelial-mesench...

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Detalles Bibliográficos
Autores: Jiménez, Natalia, Reig, Òscar, Montalbo, Ruth, Milà-Guasch, Maria, Nadal-Dieste, Lluis, Castellano, Giancarlo, Lozano, Juan José, Victoria, Iván, Font, Albert, Rodriguez-Vida, Alejo, Carles, Joan, Suárez, Cristina, Doménech, Montserrat, Sala-González, Núria, Fernández, Pedro Luís, Rodríguez-Carunchio, Leonardo, Díaz, Sherley, Prat, Aleix, Marín-Aguilera, Mercedes, Mellado, Begoña
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2020
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:10230/48155
Acceso en línea:http://hdl.handle.net/10230/48155
http://dx.doi.org/10.3389/fonc.2020.594023
Access Level:acceso abierto
Palabra clave:EMT—epithelial-mesenchymal transition
Cabazitaxel
Castration-resistant prostate cancer
Cell plasticity
Docetaxel
Neuroendocrine
Taxanes resistance
Descripción
Sumario:The prostatic tumor cells plasticity is involved in resistance to hormone-therapy, allowing these cells to survive despite androgen receptor inhibition. However, its role in taxanes resistance has not been fully established. Gene expression of plasticity-related phenotypes such as epithelial-mesenchymal transition (EMT), stem cell-like and neuroendocrine (NE) phenotypes was studied in vitro, in silico, in circulating tumor cells (CTCs) (N=22) and in tumor samples (N=117) from taxanes-treated metastatic castration-resistant prostate cancer (mCRPC) patients. Docetaxel (D)-resistant cells presented a more pronounced EMT phenotype than cabazitaxel (CZ)-resistant cells. In silico analysis revealed ESRP1 down-regulation in taxane-exposed mCRPC samples. Cell plasticity-related changes occurred in CTCs after taxanes treatment. Tumor EMT phenotype was associated with lower PSA progression-free survival (PFS) to D (P<0.001), and better to CZ (P=0.002). High ESRP1 expression was independently associated with longer PSA-PFS (P<0.001) and radiologic-PFS (P=0.001) in D and shorter PSA-PFS in the CZ cohort (P=0.041). High SYP expression was independently associated with lower PSA-PFS in D (P=0.003) and overall survival (OS) in CZ (P=0.002), and high EZH2 expression was associated with adverse OS in D-treated patients (P=0.013). In conclusion, EMT profile in primary tumor is differentially associated with D or CZ benefit and NE dedifferentiation correlates with adverse taxanes clinical outcome.