Abstract:
:Although high c-Myc protein expression is observed alongside MYC amplification in some cancers, in most cases protein overexpression occurs in the absence of gene amplification, e.g., T cell lymphoma (TCL). Here, Ca2+/calmodulin-dependent protein kinase II γ (CAMKIIγ) was shown to stabilize the c-Myc protein by directly phosphorylating it at serine 62 (S62). Furthermore, CAMKIIγ was shown to be essential for tumor maintenance. Inhibition of CAMKIIγ with a specific inhibitor destabilized c-Myc and reduced tumor burden. Importantly, high CAMKIIγ levels in patient TCL specimens correlate with increased c-Myc and pS62-c-Myc levels. Together, the CAMKIIγ:c-Myc axis critically influences the development and maintenance of TCL and represents a potential therapeutic target for TCL.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Gu Y,Zhang J,Ma X,Kim BW,Wang H,Li J,Pan Y,Xu Y,Ding L,Yang L,Guo C,Wu X,Wu J,Wu K,Gan X,Li G,Li L,Forman SJ,Chan WC,Xu R,Huang Wdoi
10.1016/j.ccell.2017.06.001subject
Has Abstractpub_date
2017-07-10 00:00:00pages
115-128.e7issue
1eissn
1535-6108issn
1878-3686pii
S1535-6108(17)30251-9journal_volume
32pub_type
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