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B-cell receptor-driven MALT1 activity regulates MYC signaling in mantle cell lymphoma.
Blood 129, 333-346 (2017)
Mantle cell lymphoma (MCL) is a mature B-cell lymphoma characterized by poor clinical outcome. Recent studies revealed the importance of B-cell receptor (BCR) signaling in maintaining MCL survival. However, it remains unclear which role MALT1, an essential component of the CARD11-BCL10-MALT1 complex that links BCR signaling to the NF-κB pathway, plays in the biology of MCL. Here we show that a subset of MCLs is addicted to MALT1, as its inhibition by either RNA or pharmacologic interference induced cytotoxicity both in vitro and in vivo. Gene expression profiling following MALT1 inhibition demonstrated that MALT1 controls an MYC-driven gene expression network predominantly through increasing MYC protein stability. Thus, our analyses identify a previously unappreciated regulatory mechanism of MYC expression. Investigating primary mouse splenocytes, we could demonstrate that MALT1-induced MYC regulation is not restricted to MCL, but represents a common mechanism. MYC itself is pivotal for MCL survival because its downregulation and pharmacologic inhibition induced cytotoxicity in all MCL models. Collectively, these results provide a strong mechanistic rationale to investigate the therapeutic efficacy of targeting the MALT1-MYC axis in MCL patients.
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2.502
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Nf-kappa-b; Paracaspase Malt1; T-cells; Activation; Cleavage; Lubac; Pathogenesis; Survival; Proliferation; Inactivation
Language
Publication Year
2017
HGF-reported in Year
2017
ISSN (print) / ISBN
0006-4971
e-ISSN
1528-0020
Journal
Blood
Quellenangaben
Volume: 129,
Issue: 3,
Pages: 333-346
Publisher
American Society of Hematology
Publishing Place
Washington
Reviewing status
Peer reviewed
Institute(s)
Research Unit Signaling and Translation (SAT)
POF-Topic(s)
30203 - Molecular Targets and Therapies
Research field(s)
Enabling and Novel Technologies
PSP Element(s)
G-509800-002
WOS ID
WOS:000396529800011
PubMed ID
27864294
Erfassungsdatum
2017-03-17