NALP3 inflammasome up-regulation and CASP1 cleavage of the glucocorticoid receptor causes glucocorticoid resistance in leukemia cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-05-04

AUTHORS

Steven W Paugh, Erik J Bonten, Daniel Savic, Laura B Ramsey, William E Thierfelder, Prajwal Gurung, R K Subbarao Malireddi, Marcelo Actis, Anand Mayasundari, Jaeki Min, David R Coss, Lucas T Laudermilk, John C Panetta, J Robert McCorkle, Yiping Fan, Kristine R Crews, Gabriele Stocco, Mark R Wilkinson, Antonio M Ferreira, Cheng Cheng, Wenjian Yang, Seth E Karol, Christian A Fernandez, Barthelemy Diouf, Colton Smith, J Kevin Hicks, Alessandra Zanut, Audrey Giordanengo, Daniel Crona, Joy J Bianchi, Linda Holmfeldt, Charles G Mullighan, Monique L den Boer, Rob Pieters, Sima Jeha, Thomas L Dunwell, Farida Latif, Deepa Bhojwani, William L Carroll, Ching-Hon Pui, Richard M Myers, R Kiplin Guy, Thirumala-Devi Kanneganti, Mary V Relling, William E Evans

ABSTRACT

Glucocorticoids are universally used in the treatment of acute lymphoblastic leukemia (ALL), and resistance to glucocorticoids in leukemia cells confers poor prognosis. To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 patients newly diagnosed with ALL and found significantly higher expression of CASP1 (encoding caspase 1) and its activator NLRP3 in glucocorticoid-resistant leukemia cells, resulting from significantly lower somatic methylation of the CASP1 and NLRP3 promoters. Overexpression of CASP1 resulted in cleavage of the glucocorticoid receptor, diminished the glucocorticoid-induced transcriptional response and increased glucocorticoid resistance. Knockdown or inhibition of CASP1 significantly increased glucocorticoid receptor levels and mitigated glucocorticoid resistance in CASP1-overexpressing ALL. Our findings establish a new mechanism by which the NLRP3-CASP1 inflammasome modulates cellular levels of the glucocorticoid receptor and diminishes cell sensitivity to glucocorticoids. The broad impact on the glucocorticoid transcriptional response suggests that this mechanism could also modify glucocorticoid effects in other diseases. More... »

PAGES

607-614

Journal

TITLE

Nature Genetics

ISSUE

6

VOLUME

47

Author Affiliations

  • 1] Hematological Malignancies Program, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. [2] Department of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • HudsonAlpha Institute for Biotechnology, Huntsville, Alabama, USA.
  • Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • Department of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • High-Performance Computing Facility, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • Department of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • 1] Hematological Malignancies Program, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. [2] Department of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. [3] Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • 1] Hematological Malignancies Program, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. [2] Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • Division of Pediatric Oncology-Hematology, Erasmus University Medical Center, Sophia Children's Hospital, Rotterdam, the Netherlands.
  • 1] Division of Pediatric Oncology-Hematology, Erasmus University Medical Center, Sophia Children's Hospital, Rotterdam, the Netherlands. [2] Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands.
  • 1] Hematological Malignancies Program, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. [2] Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
  • Centre for Rare Diseases and Personalized Medicine, University of Birmingham, Birmingham, UK.
  • New York University Cancer Institute, New York University Langone Medical Center, New York, New York, USA.
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng.3283

    DOI

    http://dx.doi.org/10.1038/ng.3283

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1023910022

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/25938942


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