Ask about this productRelated genes to: FOXA1 antibody
- Gene:
- FOXA1 NIH gene
- Name:
- forkhead box A1
- Previous symbol:
- HNF3A
- Synonyms:
- -
- Chromosome:
- 14q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-11
- Date modifiied:
- 2015-02-02
Related products to: FOXA1 antibody
Related articles to: FOXA1 antibody
- FOXA1 is a pioneer transcription factor that shapes lineage-specific regulatory programs in hormone-associated cancers. Here, we integrated FOXA1 cistromes, transcriptomes, GWAS loci, expression-associated quantitative trait loci (eQTL) datasets, clinical cohorts, and functional assays to examine how FOXA1-directed transcriptional networks contribute to prostate and breast cancer biology. We identified high-confidence FOXA1 direct target genes that converge on shared oncogenic pathways while retaining cancer-type-specific regulatory modules. These FOXA1-associated transcriptional programs generated prognostic signatures that stratified patient outcomes across independent cohorts. In prostate cancer, cancer-risk variants were enriched within FOXA1 binding regions, and selected functional variants modulated FOXA1 occupancy and downstream key effector gene (, , and ) expression. Functional validation supported roles for these genetically regulated targets in prostate cancer cell proliferation and migration. Together, our findings connect inherited noncoding variation, FOXA1 chromatin binding, transcriptional regulation, and tumor-associated phenotypes, providing a framework for understanding FOXA1-centered regulatory mechanisms in hormone-associated cancers. - Source: PubMed
Publication date: 2026/08/06
Luo BinjieZhang QinYang XiayunTan ZenglaiQin LongguangYang YuehongJokela RiittaGiannareas NikolaosManninen AkiWei Gong-Hong - To analyze the type and frequency druggable mutations in patients with progressive metastatic castration-resistant prostate cancer (mCRPC). - Source: PubMed
Publication date: 2026/08/13
Steenbock OliviaRieger ConstantinHeidenreich JulianPaffenholz PiaPfister DavidBrandenstein Melanie vonHeidenreich Axel - Transcription factor SNAI1 guides plasticity and invasiveness in cancer. Using a complete SNAI1 knockout in mesenchymal, triple-negative breast cancer cells, unbiased genome-wide transcriptomic analysis revealed a marked under-expression of integrin-based adhesion and endocytic components. Utilizing this knockout cell model, complementary breast cancer cell models and functional screening of multiple differentially expressed genes, we found that the pioneering transcription factor FOXA1, whose expression is repressed by SNAI1, associates with several key mediators of the cellular phenotype. FOXA1 represses the small GTPase ARF6 and its exchange factor PSD4. In addition, some of the integrin and matrix metalloproteinase genes are regulated by the transcriptional FOXA1 signal. Accordingly, SNAI1 knockout cells presented poor adhesion to collagen type I or fibronectin, formed defective invadopodia and focal adhesions with weakened FAK/SRC signaling. SNAI1 knockout cells performed ineffective receptor-mediated internalization, including nanoparticle and extracellular vesicle (EV) uptake, exhibited reduced lysosomal content, lacked multivesicular bodies enriched in intraluminal vesicles and showed decreased EV secretion. Gain-of-function experiments demonstrated that SNAI1 has an impact on the PSD4/ARF6 signaling module, using FOXA1 as an intermediate factor to regulate EV release by tumor cells. We propose that the SNAI1-FOXA1 transcriptional mechanism operates at the level of membrane and vesicular trafficking control, which interlinks cell plasticity, adhesion and invasiveness through the extracellular environment, with the associated process of EV secretion. - Source: PubMed
Publication date: 2026/08/12
Tsirigoti ChrysoulaAli Mohamad MoustafaMorén AnitaJohansson StaffanMunson Michael JHeldin Carl-HenrikMoustakas AristidisRodrigues-Junior Dorival Mendes - 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. This study aims to identify novel drivers of SCLC chemoresistance. - Source: PubMed
Publication date: 2026/06/10
Pan DeshenWei KeihongSheng LuoyanGao QingXu ChaoliangXi YufeiJia DeshuiZhang Yan - The carcinogenic mechanism of benzo[a]pyrene (BaP) is not fully understood. Our previous studies unexpectedly revealed that A-kinase anchoring protein 12 (AKAP12), a recognized tumor suppressor frequently downregulated in malignancies, is markedly upregulated in BaP-transformed 16HBE cells (THBEc1). This paradoxical upregulation prompted us to investigate its functional consequence and regulatory mechanism. Using CRISPR/Cas9-mediated genome editing, we serendipitously obtained a cell line harboring a homozygous 18-bp deletion at positions 61 to 78 in exon 3 of AKAP12, resulting in loss of six amino acids and sustained upregulation of mutant protein; this line was named THBEc1-ΔAKAP12-c4. These cells exhibited decreased in vitro colony growth and migration, and decreased in vivo experimental lung metastasis, without affecting subcutaneous tumor growth, revealing selective suppression of metastatic phenotypes. Furthermore, we identified forkhead box A1 (FOXA1), a transcription factor with an established oncogenic role in BaP-induced carcinogenesis, as a key upstream regulator: knockout of FOXA1 downregulated AKAP12. These findings outline a dual role for FOXA1 in driving oncogenic processes while upregulating AKAP12 as a compensatory brake on metastasis. Our study supports the tumor/metastasis suppressor role of AKAP12 in BaP-induced carcinogenesis, and the mutant AKAP12 provides a tool for dissecting the functional domains of this protein. - Source: PubMed
Publication date: 2026/08/03
Hao MingmeiFu YujinLin YitongWang YuLi LudiFu DaweiYao BiyunFu JuanlingZhou ZongcanSu JingZhao Peng