Fosl1 is a transcriptional effector of <i>BRAF</i> ^V600E-driven intestinal tumorigenesis.

ABSTRACT: The serrated neoplasia pathway is an alternate route to colorectal cancer (CRC) development where BRAF ^V600E is the most common initiating genetic alteration. BRAF^V600E-driven tumorigenesis requires gene expression changes mediated by activation of the ERK MAPK signaling pathway. However, the key effectors of this process are elusive. Here, we identify the ERK-regulated transcription factor Fosl1, one such effector. We show that Fosl1 is dispensable for the initiation of BRAF^V600E-driven serrated neoplasia in mice but promotes progression of the disease by regulating the expression of genes involved in inflammation, immunity, cell cycle control, fetal-like programming, and gastric metaplasia. Notably, transgenic Fosl1 expression alone was sufficient

SUBMITTER: Alam Z 

PROVIDER: S-EPMC12661198 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature