Phosphorylation deficient inducible cAMP early repressor (ICER) modulates tumorigenesis and survival in a transgenic zebrafish (Danio rerio) model of melanoma.

ABSTRACT: Melanoma, the most lethal form of skin cancer, is commonly associated with mutations in the BRAF gene, particularly BRAFV600E, which drives tumor proliferation via the ERK1/2 signaling cascade. While BRAF inhibitors initially demonstrate efficacy, therapeutic resistance remains a significant challenge. Emerging evidence implicates the cAMP signaling pathway, particularly the cAMP response element-binding protein (CREB) and its repressor, inducible cAMP early repressor (ICER), in melanoma progression and drug resistance. ICER, a transcriptional repressor regulated via Ras/MAPK-mediated phosphorylation and ubiquitination, is degraded in melanoma, undermining its tumor-suppressive role. In a brafV600E; p53 (loss of function) transgenic zebrafish (Danio rerio) model, we investigated the role o

SUBMITTER: Wheelan J 

PROVIDER: S-EPMC12381921 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature