GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE313nnn/GSE313394/primaryOK200GenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE313394GEOGSEfalseFOXA1 promotes SCLC chemoresistance [ChIP-Seq]Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor. While chemotherapy has been the cornerstone of first-line treatment, most SCLC patients develop chemoresistance shortly after an initial response, and the molecular basis of this resistance remains poorly understood. Here, we identify FOXA1 as a frequently amplified and upregulated gene in SCLC, with high FOXA1 expression correlating with poor outcomes. We further demonstrate that FOXA1 overexpression promotes resistance to chemotherapy. Mechanistically, we reveal that WNT5A is a downstream target of FOXA1 that mediates chemoresistance through activation of the Wnt/β-catenin pathway. FOXA1 also induces epithelial-mesenchymal transition (EMT) in SCLC cells, and human SCLC tumors with high FOXA1 expression exhibit enriched EMT and Wnt/β-catenin pathway signatures. Importantly, pharmacological inhibition of the Wnt pathway selectively suppresses the growth of FOXA1-overexpressing SCLC cells. Collectively, our study identifies FOXA1 as a key driver of chemoresistance in SCLC and highlights Wnt pathway inhibition as a promising strategy to overcome FOXA1-driven chemoresistance.2026/09/23GSE313394GSM9367380GSM936737924676313394Homo sapiens