Beclin 1 restrains tumorigenesis through Mcl-1 destabilization in an autophagy-independent reciprocal manner View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-12

AUTHORS

Mohamed Elgendy, Marco Ciro, Amal Kamal Abdel-Aziz, Giuseppe Belmonte, Roberto Dal Zuffo, Ciro Mercurio, Clelia Miracco, Luisa Lanfrancone, Marco Foiani, Saverio Minucci

ABSTRACT

Mcl-1 is a unique Bcl-2 family member that plays crucial roles in apoptosis. Apoptosis-unrelated functions of Mcl-1 are however emerging, further justifying its tight regulation. Here we unravel a novel mechanism of Mcl-1 regulation mediated by the haplo-insufficient tumour suppressor Beclin 1. Beclin 1 negatively modulates Mcl-1 stability in a reciprocal manner whereby depletion of one leads to the stabilization of the other. This co-regulation is independent of autophagy and of their physical interaction. Both Beclin 1 and Mcl-1 are deubiquitinated and thus stabilized by binding to a common deubiquitinase, USP9X. Beclin 1 and Mcl-1 negatively modulate the proteasomal degradation of each other through competitive displacement of USP9X. The analysis of patient-derived melanoma cells and tissue samples shows that the levels of Beclin 1 decrease, while Mcl-1 levels subsequently increase during melanoma progression in a significant inter-dependent manner. The identified inverse co-regulation of Beclin 1 and Mcl-1 represents a mechanism of functional counteraction in cancer. More... »

PAGES

5637

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms6637

DOI

http://dx.doi.org/10.1038/ncomms6637

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031661101

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25472497


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