ArticleIn vivo (Athens, Greece)
FOXA1 Alterations in Prostate Cancer: Expression, Mutation Classes, and Copy Number Changes.
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Abstract
BACKGROUND/
aimProstate cancer features profound transcriptional dysregulation within the androgen receptor (AR) signaling axis. The pioneer factor FOXA1, which facilitates AR binding to chromatin, is recurrently altered in 10-40% of tumors. Recent studies classify FOXA1 mutations as Class 1 Wing 2 mutations, which enhance AR-dependent tumorigenesis, and Class 2 C-terminal truncations, which promote lineage plasticity and therapy resistance. The interplay of FOXA1 alterations with TMPRSS2-ERG fusions and PROX1 remains incompletely understood. MATERIALS AND
methodsData from The Cancer Genome Atlas (TCGA) Prostate Adenocarcinoma (PRAD) cohort (n=492) were analyzed
resultsFOXA1 was broadly expressed, with subsets showing elevation. Class 1 mutations localized to the Wing 2 region, while Class 2 truncations clustered in the C-terminal domain. Copy number changes were infrequent, indicating mutation-driven reprogramming as the main oncogenic mechanism. TMPRSS2 and ERG strongly co-occurred (log2 OR >3,
conclusionFOXA1 defines a major oncogenic axis in prostate cancer, distinct from TMPRSS2-ERG fusion and PROX1 induction. Class 1 and 2 FOXA1 mutations drive alternative transcriptional programs leading to therapy resistance, highlighting FOXA1 as a critical biomarker and target for chromatin-directed interventions.
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