CAMKV Kinase Signaling Is a Novel Therapeutic Avenue with Prognostic Relevance in Neuroblastoma

Tumor progression is frequently driven by MYCN amplification or MYC overexpression, yet direct pharmacologic targeting of these oncogenic transcription factors has proven challenging. Here, we identify CaM kinase-like vesicle-associated protein (CAMKV), previously considered a pseudokinase, as a MYCN/MYC-regulated kinase that promotes NB tumor growth.

Genetic depletion of CAMKV inhibited NB cell proliferation and suppressed tumor growth in vivo. Bioinformatic analyses and immunohistochemical staining of primary tumors revealed that elevated CAMKV expression correlates with poor patient survival. Integrated proteomic and transcriptomic profiling demonstrated that CAMKV regulates oncogenic signaling networks essential for NB pathogenesis.