PLX090118

GSE99364: Stabilization of c-Myc protein by CAMKII promotes T-cell lymphoma

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

Although high c-Myc protein expression is observed alongside c-Myc gene amplification in some cancers, in most cases protein overexpression occurs while the amplified gene is largely absent, e.g. T-cell lymphoma (TCL). Here, Ca2+/calmodulin-dependent protein kinase II (CAMKII) was shown to stabilize c-Myc protein by directly phosphorylating at serine 62 (S62), which represents a hitherto unknown mechanism of c-Myc protein overexpression. Further, CAMKII was shown to be essential for tumor maintenance. Inhibiting CAMKII with a potent CAMKII-specific inhibitor destabilized c-Myc and reduced tumor burden dramatically. Importantly, high CAMKII in clinical patient specimens positively correlated with increased c-Myc / pS62-c-Myc expression. Together, the CAMKII:c-Myc axis critically influences the development and maintenance of TCL, and represent a novel therapeutic target for TCL. SOURCE: LU YANG (luyang@coh.org) - city of hope