期刊
FRONTIERS IN ONCOLOGY
卷 8, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2018.00498
关键词
CARMA1; CARD11; BCL10; MALT1; CBM; post-translational modifications; diffuse large B-cell lymphoma; ABC DLBCL
类别
资金
- Fondation pour la Recherche Medicale [DEQ20180339184]
- Fondation ARC pour la Recherche sur le Cancer
- Ligue nationale contre le cancer comites de Loire-Atlantique, Maine et Loire, Vendee, Region Pays de la Loire et Nantes Metropole under Connect Talent Grant
- Fondation ARC
- Nantes Metropole
Piracy of the NF-kappa B transcription factors signaling pathway, to sustain its activity, is a mechanism often deployed in B-cell lymphoma to promote unlimited growth and survival. The aggressive activated B-cell like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) exploits a multi-protein complex of CARMA1, BCL10, and MALT1 (CBM complex), which normally conveys NF-kappa B signaling upon antigen receptors engagement. Once assembled, the CBM also unleashes MALT1 protease activity to finely tune the immune response. As a result, ABC DLBCL tumors develop a profound addiction to NF-kappa B and to MALT1 enzyme, leaving open a breach for therapeutics. However, the pleiotropic nature of NF-kappa B jeopardizes the success of its targeting and urges us to develop new strategies. In this review, we discuss how post-translational modifications, such as phosphorylation and ubiquitination of the CBM components, as well as, MALT1 proteolytic activity, shape the CBM activity in lymphocytes and ABC DLBCL, and may provide new avenues to restore vulnerability in lymphoma.
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