MET inhibition overcomes radiation resistance of glioblastoma stem‐like cells

Abstract Glioblastoma (GBM) contains stem‐like cells (GSCs) known to be resistant to ionizing radiation and thus responsible for therapeutic failure and rapidly lethal tumor recurrence. It is known that GSC radioresistance relies on efficient activation of the DNA damage response, but the mechanisms...

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Main Authors: Francesca De Bacco, Antonio D'Ambrosio, Elena Casanova, Francesca Orzan, Roberta Neggia, Raffaella Albano, Federica Verginelli, Manuela Cominelli, Pietro L Poliani, Paolo Luraghi, Gigliola Reato, Serena Pellegatta, Gaetano Finocchiaro, Timothy Perera, Elisabetta Garibaldi, Pietro Gabriele, Paolo M Comoglio, Carla Boccaccio
Format: Article
Language:English
Published: Springer Nature 2016-04-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.201505890
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author Francesca De Bacco
Antonio D'Ambrosio
Elena Casanova
Francesca Orzan
Roberta Neggia
Raffaella Albano
Federica Verginelli
Manuela Cominelli
Pietro L Poliani
Paolo Luraghi
Gigliola Reato
Serena Pellegatta
Gaetano Finocchiaro
Timothy Perera
Elisabetta Garibaldi
Pietro Gabriele
Paolo M Comoglio
Carla Boccaccio
author_facet Francesca De Bacco
Antonio D'Ambrosio
Elena Casanova
Francesca Orzan
Roberta Neggia
Raffaella Albano
Federica Verginelli
Manuela Cominelli
Pietro L Poliani
Paolo Luraghi
Gigliola Reato
Serena Pellegatta
Gaetano Finocchiaro
Timothy Perera
Elisabetta Garibaldi
Pietro Gabriele
Paolo M Comoglio
Carla Boccaccio
author_sort Francesca De Bacco
collection DOAJ
description Abstract Glioblastoma (GBM) contains stem‐like cells (GSCs) known to be resistant to ionizing radiation and thus responsible for therapeutic failure and rapidly lethal tumor recurrence. It is known that GSC radioresistance relies on efficient activation of the DNA damage response, but the mechanisms linking this response with the stem status are still unclear. Here, we show that the MET receptor kinase, a functional marker of GSCs, is specifically expressed in a subset of radioresistant GSCs and overexpressed in human GBM recurring after radiotherapy. We elucidate that MET promotes GSC radioresistance through a novel mechanism, relying on AKT activity and leading to (i) sustained activation of Aurora kinase A, ATM kinase, and the downstream effectors of DNA repair, and (ii) phosphorylation and cytoplasmic retention of p21, which is associated with anti‐apoptotic functions. We show that MET pharmacological inhibition causes DNA damage accumulation in irradiated GSCs and their depletion in vitro and in GBMs generated by GSC xenotransplantation. Preclinical evidence is thus provided that MET inhibitors can radiosensitize tumors and convert GSC‐positive selection, induced by radiotherapy, into GSC eradication.
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publishDate 2016-04-01
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spelling doaj-art-e3a220eeaa804cb09dc87829df92d2bd2025-08-20T04:02:55ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842016-04-018555056810.15252/emmm.201505890MET inhibition overcomes radiation resistance of glioblastoma stem‐like cellsFrancesca De Bacco0Antonio D'Ambrosio1Elena Casanova2Francesca Orzan3Roberta Neggia4Raffaella Albano5Federica Verginelli6Manuela Cominelli7Pietro L Poliani8Paolo Luraghi9Gigliola Reato10Serena Pellegatta11Gaetano Finocchiaro12Timothy Perera13Elisabetta Garibaldi14Pietro Gabriele15Paolo M Comoglio16Carla Boccaccio17Laboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSDepartment of Molecular and Translational Medicine, Pathology Unit, University of BresciaDepartment of Molecular and Translational Medicine, Pathology Unit, University of BresciaLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSUnit of Molecular Neuro‐Oncology, Fondazione IRCCS Istituto Neurologico C. BestaUnit of Molecular Neuro‐Oncology, Fondazione IRCCS Istituto Neurologico C. BestaOctimet Oncology Ltd.Unit of Radiotherapy, Candiolo Cancer Institute, FPO‐IRCCSUnit of Radiotherapy, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSLaboratory of Cancer Stem Cell Research, Candiolo Cancer Institute, FPO‐IRCCSAbstract Glioblastoma (GBM) contains stem‐like cells (GSCs) known to be resistant to ionizing radiation and thus responsible for therapeutic failure and rapidly lethal tumor recurrence. It is known that GSC radioresistance relies on efficient activation of the DNA damage response, but the mechanisms linking this response with the stem status are still unclear. Here, we show that the MET receptor kinase, a functional marker of GSCs, is specifically expressed in a subset of radioresistant GSCs and overexpressed in human GBM recurring after radiotherapy. We elucidate that MET promotes GSC radioresistance through a novel mechanism, relying on AKT activity and leading to (i) sustained activation of Aurora kinase A, ATM kinase, and the downstream effectors of DNA repair, and (ii) phosphorylation and cytoplasmic retention of p21, which is associated with anti‐apoptotic functions. We show that MET pharmacological inhibition causes DNA damage accumulation in irradiated GSCs and their depletion in vitro and in GBMs generated by GSC xenotransplantation. Preclinical evidence is thus provided that MET inhibitors can radiosensitize tumors and convert GSC‐positive selection, induced by radiotherapy, into GSC eradication.https://doi.org/10.15252/emmm.201505890glioblastomaglioblastoma stem‐like cellsMET oncogeneradiosensitizationradiotherapy
spellingShingle Francesca De Bacco
Antonio D'Ambrosio
Elena Casanova
Francesca Orzan
Roberta Neggia
Raffaella Albano
Federica Verginelli
Manuela Cominelli
Pietro L Poliani
Paolo Luraghi
Gigliola Reato
Serena Pellegatta
Gaetano Finocchiaro
Timothy Perera
Elisabetta Garibaldi
Pietro Gabriele
Paolo M Comoglio
Carla Boccaccio
MET inhibition overcomes radiation resistance of glioblastoma stem‐like cells
EMBO Molecular Medicine
glioblastoma
glioblastoma stem‐like cells
MET oncogene
radiosensitization
radiotherapy
title MET inhibition overcomes radiation resistance of glioblastoma stem‐like cells
title_full MET inhibition overcomes radiation resistance of glioblastoma stem‐like cells
title_fullStr MET inhibition overcomes radiation resistance of glioblastoma stem‐like cells
title_full_unstemmed MET inhibition overcomes radiation resistance of glioblastoma stem‐like cells
title_short MET inhibition overcomes radiation resistance of glioblastoma stem‐like cells
title_sort met inhibition overcomes radiation resistance of glioblastoma stem like cells
topic glioblastoma
glioblastoma stem‐like cells
MET oncogene
radiosensitization
radiotherapy
url https://doi.org/10.15252/emmm.201505890
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