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
- Nonalcoholic steatohepatitis (NASH) is characterized by hepatocyte injury and lobular inflammation driven by lipid accumulation, oxidative stress, and apoptosis. Low testosterone levels are associated with increased steatosis risk, particularly in transgender women undergoing feminization. To investigate the effects of estradiol supplementation and its mechanisms involving lipid metabolism, oxidative stress, apoptosis, and mitogen-activated protein kinase (MAPK) signaling (ERK, JNK, and p38) in testosterone-deficient rats fed a high-fat, high-fructose (HFHF) diet. Twenty-one male Sprague-Dawley rats were randomized into three groups ( = 7/group): (i) control (standard diet), (ii) ORX + HFHF (bilateral orchidectomy plus HFHF diet), and (iii) ORX + HFHF + E2 (ORX + HFHF plus oral estradiol, 1.6 mg/kg/day). After 6 weeks, the ORX + HFHF group exhibited the greatest hepatic steatosis, lobular inflammation, hepatocyte ballooning, NAS scores, and Oil Red O staining. Lipid accumulation markers (PLIN2 and Foxa1), oxidative stress markers (MDA, 4-hydroxynonenal, HO-1, and iNOS), and Nrf2 expression were significantly increased versus controls. Testosterone deficiency combined with HFHF feeding induced apoptosis primarily through the intrinsic pathway, evidenced by increased Bax, Bcl-2, caspase-3, and caspase-9, while caspase-8 showed an increasing trend. Estradiol supplementation significantly attenuated NASH pathology by reducing lipogenesis, oxidative stress, and apoptosis, with these effects strongly associated with suppression of all MAPK subtypes. Estradiol mitigates NASH progression in testosterone-deficient rats by modulating lipid metabolism, restoring antioxidant defenses, suppressing intrinsic apoptosis, and inhibiting MAPK signaling. These findings provide mechanistic insight into hormone therapy in transgender women and identify GPER/MAPK signaling as a potential therapeutic target. - Source: PubMed
Publication date: 2026/09/01
Okrit FatistChayanupatkul ManeeratWanpiyarat NatchaSiriviriyakul PrasongWerawatganon Duangporn - Breast cancer (BC), the most widespread malignancy in women globally, is characterized by complex and heterogeneous mechanisms. Lectin, mannose binding 2 (LMAN2), a potential oncogene highly expressed in BC, is linked to poor prognosis. The transcription factor forkhead box protein A1 (FOXA1) is often overexpressed in BC and tied to malignant phenotypes, but how it regulates LMAN2 to influence BC progression remains unclear. - Source: PubMed
Publication date: 2026/08/22
Zhang ZhitaoWang ShaoyunSun HaifengYu Yinping - Previous genome-wide association studies have identified more than 400 prostate cancer (PCa) susceptibility loci. However, the tissue and spatial epithelial contexts through which inherited PCa risk may operate in the normal prostate remain incompletely understood. We analyzed normal human prostate spatial transcriptomic data using a gsMap-based framework to localize PCa association signals across spatially resolved prostate compartments. Spatial spots were clustered using SpaGCN and then manually curated and annotated based on matched histological images and canonical prostate marker gene expression. Because individual spatial spots may contain multiple cells, annotations were interpreted as compartment-enriched dominants rather than pure cell-type identities. PCa genetic association scores were aggregated within annotated compartments using Cauchy-combined p value and median spot-level p value as a complementary descriptive summary. Gene-level spatial correspondence was further assessed using Pearson correlation coefficients (PCCs) between gene-expression patterns and spot-level PCa gsMap signal. We annotated normal prostate tissue into four major compartments: basal epithelium-enriched, luminal epithelium-enriched, smooth muscle-enriched, and fibroblast stroma-enriched compartments. Basal epithelium-enriched compartments showed the strongest and most consistent enrichment for PCa association, with a Cauchy-combined p of 1.85 × 10 and a median spot-level based p of 3.67 × 10. Luminal epithelium-enriched compartments also showed strong enrichment, with a Cauchy p of 3.79 × 10 and a median-based p of 1.45 × 10. In contrast, fibroblast stroma-enriched compartments showed no evidence of enrichment (Cauchy p = 0.52; median p = 0.42), while smooth muscle-enriched compartments showed only modest evidence in the Cauchy-based analysis that was accompanied by a weaker median spot-level association signal (Cauchy p = 8.95 × 10; median p = 0.18). PCC analysis showed that genes with the strongest spatial correspondence to PCa gsMap signal were predominantly epithelial-associated, including CDH1, VAMP8, GMNN, TSPAN1, and FOXA1. In normal human prostate tissue, inherited PCa association localizes preferentially to basal epithelium-enriched and luminal epithelial-enriched compartments rather than to smooth muscle-enriched or fibroblast stroma-enriched compartments. Gene-level PCC patterns further support spatial alignment between PCa-associated gsMap signal and epithelial transcriptional programs. These findings provide proof-of-concept evidence for the spatial localization of inherited PCa susceptibility through the integration of large-scale population-based genetic data and spatial transcriptomics. - Source: PubMed
Publication date: 2026/08/30
Liu ShuaiChan Owen T MZhong HuaShahabi AliWu LangZhu Jingjing - Lipophagy-driven metabolic reprogramming is increasingly recognized as a determinant of tumor progression. TRIB3, a key regulator of lipid metabolism, has been implicated in cancer aggressiveness, with elevated expression linked to poor outcomes in triple-negative breast cancer. Here, we investigated whether TRIB3 promotes TNBC metastasis through regulation of lipophagy and lipid metabolism. - Source: PubMed
Publication date: 2026/08/29
Ruan LiqiongLiu JianfengJiang Zirong - To investigate the mechanism of Placenta-specific 8 (PLAC8) in the tumor microenvironment (TME) of breast cancer. - Source: PubMed
Publication date: 2026/08/14
Yu Mengqi