C-Met/MIR-130b axis as novel mechanism and biomarker for castration resistance state acquisition

A. Cannistraci, G. Federici, A. Addario, A. L. Di Pace, L. Grassi, G. Muto, D. Collura, M. Signore, L. De Salvo, S. Sentinelli, G. Simone, M. Costantini, Emanuele Maria Costantini, Simona Nanni, A. Farsetti, Antonella Farsetti, V. Coppola, Valeria Coppola, Ruggero De Maria Marchiano, D. Bonci

Research output: Contribution to journalArticle

24 Citations (Scopus)


Although a significant subset of prostate tumors remain indolent during the entire life, the advanced forms are still one of the leading cause of cancer-related death. There are not reliable markers distinguishing indolent from aggressive forms. Here we highlighted a new molecular circuitry involving microRNA and coding genes promoting cancer progression and castration resistance. Our preclinical and clinical data demonstrated that c-Met activation increases miR-130b levels, inhibits androgen receptor expression, promotes cancer spreading and resistance to hormone ablation therapy. The relevance of these findings was confirmed on patients' samples and by in silico analysis on an independent patient cohort from Taylor's platform. Data suggest c-Met/miR-130b axis as a new prognostic marker for patients' risk assessment and as an indicator of therapy resistance. Our results propose new biomarkers for therapy decision-making in all phases of the pathology. Data may help identify high-risk patients to be treated with adjuvant therapy together with alternative cure for castration-resistant forms while facilitating the identification of possible patients candidates for anti-Met therapy. In addition, we demonstrated that it is possible to evaluate Met/miR-130b axis expression in exosomes isolated from peripheral blood of surgery candidates and advanced patients offering a new non-invasive tool for active surveillance and therapy monitoring.
Original languageEnglish
Pages (from-to)3718-3728
Number of pages11
Publication statusPublished - 2017


  • Animals
  • Biomarkers, Tumor
  • Cancer Research
  • Cell Line, Tumor
  • Disease Progression
  • Genetics
  • Heterografts
  • Humans
  • Male
  • Mice
  • Mice, Inbred NOD
  • MicroRNAs
  • Molecular Biology
  • Prostatic Neoplasms
  • Prostatic Neoplasms, Castration-Resistant
  • Proto-Oncogene Proteins c-met


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