MST1/Hippo promoter gene methylation predicts poor survival in patients with malignant pleural mesothelioma in the IFCT-GFPC-0701 MAPS Phase 3 trial View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-02-11

AUTHORS

Elodie Maille, Solenn Brosseau, Vincent Hanoux, Christian Creveuil, Claire Danel, Emmanuel Bergot, Arnaud Scherpereel, Julien Mazières, Jacques Margery, Laurent Greillier, Clarisse Audigier-Valette, Denis Moro-Sibilot, Olivier Molinier, Romain Corre, Isabelle Monnet, Valérie Gounant, Alexandra Langlais, Franck Morin, Guénaëlle Levallet, Gérard Zalcman

ABSTRACT

BACKGROUND: The Mesothelioma Avastin Cisplatin Pemetrexed Study (MAPS/NCT00651456) phase 3 trial demonstrated the superiority of bevacizumab plus pemetrexed-cisplatin triplet over chemotherapy alone in 448 malignant pleural mesothelioma (MPM) patients. Here, we evaluated the prognostic role of Hippo pathway gene promoter methylation. METHODS: Promoter methylations were assayed using methylation-specific polymerase chain reaction in samples from 223 MAPS patients, evaluating their prognostic value for overall survival (OS) and disease-free survival in univariate and multivariate analyses. MST1 inactivation effects on invasion, soft agar growth, apoptosis, proliferation, and YAP/TAZ activation were investigated in human mesothelial cell lines. RESULTS: STK4 (MST1) gene promoter methylation was detected in 19/223 patients tested (8.5%), predicting poorer OS in univariate and multivariate analyses (adjusted HR: 1.78, 95% CI (1.09-2.93), p = 0.022). Internal validation by bootstrap resampling supported this prognostic impact. MST1 inactivation reduced cellular basal apoptotic activity while increasing proliferation, invasion, and soft agar or in suspension growth, resulting in nuclear YAP accumulation, yet TAZ cytoplasmic retention in mesothelial cell lines. YAP silencing decreased invasion of MST1-depleted mesothelial cell lines. CONCLUSIONS: MST1/hippo kinase expression loss is predictive of poor prognosis in MPM patients, leading to nuclear YAP accumulation and electing YAP as a putative target for therapeutic intervention in human MPM. More... »

PAGES

387-397

Journal

TITLE

British Journal of Cancer

ISSUE

4

VOLUME

120

Author Affiliations

  • Normandie Université, UNICAEN, CEA, CNRS, ISTCT/CERVOxy group, GIP CYCERON, Caen, France
  • Department of Thoracic Oncology & CIC1425, Hôpital Bichat-Claude Bernard, Assistance Publique Hôpitaux de Paris, Université Paris-Diderot, Paris, France
  • Normandie Université, UNICAEN, UPRES-EA 2608, Caen, France
  • Biomedical Research Unit, CHU de Caen, Caen, France
  • Department of Pathology, Hôpital Bichat-Claude Bernard, AP-HP, Université Paris-Diderot, Paris, France
  • Department of Pulmonology & Thoracic Oncology, CHU de Caen, Caen, France
  • Department of Pulmonary and Thoracic Oncology, Centre Hospitalier Universitaire Lille, University of Lille, U1019 INSERM, Center of Infection and Immunity of Lille, Lille, France
  • Department of Pulmonology, Hôpital Larrey, University Hospital of Toulouse, Toulouse, France
  • Medical Oncology Department, Gustave Roussy, Villejuif, France
  • Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM UMR1068, CNRS UMR7258, Aix-Marseille University, UM105 Marseille, France
  • Department of Pulmonology, Centre Hospitalier Toulon Sainte-Musse, Toulon, France
  • Pôle Thorax et Vaisseaux, Centre Hospitalier Universitaire Grenoble, Grenoble, France
  • Department of Pulmonology, Centre Hospitalier Le Mans, Le Mans, France
  • Department of Pulmonology, Pontchaillou University Hospital, Rennes, France
  • Department of Pulmonology, Centre Hospitalier Intercommunal Créteil, Créteil, France
  • Department of Pulmonology, Hôpital Tenon, Assistance Publique Hôpitaux de Paris, Paris, France
  • Intergroupe Francophone de Cancérologie Thoracique (IFCT), Paris, France
  • Department of Pathology, CHU de Caen, Caen, France
  • U830 INSERM “Genetics and Biology of Cancers, A.R.T group”, Curie Institute, Paris, France
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41416-019-0379-8

    DOI

    http://dx.doi.org/10.1038/s41416-019-0379-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112039417

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30739911


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