| Literature DB >> 28697340 |
Ying Gu1, Jiawei Zhang1, Xiaoxiao Ma2, Byung-Wook Kim2, Hailong Wang1, Jinfan Li3, Yi Pan4, Yang Xu5, Lili Ding1, Lu Yang6, Chao Guo6, Xiwei Wu6, Jun Wu7, Kirk Wu1, Xiaoxian Gan1, Gang Li1, Ling Li8, Stephen J Forman9, Wing-Chung Chan10, Rongzhen Xu11, Wendong Huang12.
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.Entities:
Keywords: CAMKIIγ; T cell lymphoma; c-MYC; c-Myc stabilization; phosphorylation
Mesh：
Substances：
Year: 2017 PMID： 28697340 PMCID： PMC5552197 DOI： 10.1016/j.ccell.2017.06.001
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743