Loss of Spry1 reduces growth of BRAF^V600-mutant cutaneous melanoma and improves response to targeted therapy.

ABSTRACT: Mitogen-activated protein kinase (MAPK) pathway activation is a central step in BRAF^V600-mutant cutaneous melanoma (CM) pathogenesis. In the last years, Spry1 has been frequently described as an upstream regulator of MAPK signaling pathway. However, its specific role in BRAF^V600-mutant CM is still poorly defined. Here, we report that Spry1 knockdown (Spry1^KO) in three BRAF^V600-mutant CM cell lines markedly induced cell cycle arrest and apoptosis, repressed cell proliferation in vitro, and impaired tumor growth in vivo. Furthermore, our findings indicated that Spry1^KO reduced the expression of several markers of epithelial-mesenchymal transition, such as MMP-2 both in vitro and in vivo. These effects were associated with a sustained and

SUBMITTER: Montico B 

PROVIDER: S-EPMC7244546 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature