Suppression of Spry1 reduces HIF1α-dependent glycolysis and impairs angiogenesis in BRAF-mutant cutaneous melanoma.

ABSTRACT:

Background

About 50% of cutaneous melanoma (CM) harbors the activating BRAF^V600 mutation which exerts most of the oncogenic effects through the MAPK signaling pathway. In the last years, a number of MAPK modulators have been identified, including Spry1. In this context, we have recently demonstrated that knockout of Spry1 (Spry1^KO) in BRAF^V600-mutant CM led to cell cycle arrest and apoptosis, repressed cell proliferation in vitro, and reduced tumor growth in vivo. Despite these findings, however, the precise molecular mechanism linking Spry1 to BRAF^V600-mutant CM remains to be elucidated.

Materials and methods

Immunoprecipitation coupled to mass spectrometry was employed to gain insight into Spry1 interactome. Spry1 gene was knocke

SUBMITTER: Montico B 

PROVIDER: S-EPMC11827140 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature