FOXA1 Mouse Monoclonal Antibody
- Known as:
- FOXA1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003169-M03
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOXA1 Mouse Monoclonal Antibody
Related genes to: FOXA1 Mouse Monoclonal 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 Mouse Monoclonal Antibody
Related articles to: FOXA1 Mouse Monoclonal Antibody
- Oral squamous cell carcinoma (OSCC) accounts for the vast majority of oral cancer cases. Accumulating evidence has implicated both AlkB homolog 5 (ALKBH5) and forkhead box protein A1 (FOXA1) in the emergence of cisplatin resistance in OSCC. This study aimed to define their functional roles and elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/06/06
Wang YingYang Hui-XinGu Yu-JiaTian MeiGeng Qi-Feng - Drug resistance frequently results in treatment failure for leukemia and leads to the progression of chronic myeloid leukemia (CML) into an accelerated or blast phase. An increasing number of CML cases exhibit reduced responsiveness or are refractory to tyrosine kinase inhibitors and chemotherapeutic drugs. Exosomes, as intercellular communication carriers, have been shown to participate in various forms of tumor drug resistance, but their role and mechanisms in CML drug resistance have not yet been fully investigated. - Source: PubMed
Publication date: 2026/06/01
Li FeiLin Jin-FeiTian PengChen HaishengYang QianGuo QiqiWang JiashengHe YueChen JunruHu XiaojianLi ChunmouMai WeitongDuan MenghanPeng MichaelRousseau ZackaryChen ChunNi HeyuZhang Qing - Adult women are typically exposed to 17β-estradiol (E2) concentrations of ~100 to 200 pM, yet most cell-based studies use 100 nM. We determined the molecular effects of E2 concentrations spanning six orders of magnitude (1 pM to 100 nM) in breast cancer cells. Estrogen receptor α (ERα) enhancers formed at low physiological doses of E2 (1 to 100 pM) are mechanistically distinct from those that form at high pharmacological doses (10 to 100 nM). They (i) form in open chromatin bound by FOXA1, (ii) are clustered within topologically associated domains, (iii) produce enhancer RNAs enriched with functional enhancer RNA regulatory motifs, and (iv) drive expression of proliferation genes with promoter-proximal paused RNA polymerase II and distinct co-regulator enrichment. Low-dose ERα enhancer usage is elevated in patients who have breast cancer with poor responses to aromatase inhibitors, likely as a continued response to low circulating levels of E2. Collectively, our results identify mechanistic differences between low- and high-dose ERα enhancers that specify distinct biological outcomes. - Source: PubMed
Publication date: 2026/06/03
Kim Hyung BumNandu TulipKim Yoon JungCamacho Cristel VKraus W Lee - Prostate cancer (PCa) is increasingly recognized to be driven by dysregulated lipid metabolism. Although fatty acid synthase (FASN) is highly expressed in PCa, the mechanisms governing FASN protein stability and its functional integration into oncogenic lipid metabolism remain poorly defined. In this study, we identified chaperonin-containing TCP1 subunit 2 (CCT2) as a key oncogenic regulator that promotes lipid synthesis and enhances malignant phenotypes both in vitro and in vivo. Mechanistically, CCT2 transcription is upregulated by the transcription factor Forkhead Box A1 (FOXA1); the CCT2 protein interacts with eukaryotic translation initiation factor 3 subunit F (EIF3F) and FASN to facilitate the assembly of a CCT2/EIF3F/FASN ternary complex. This complex enhances the EIF3F-mediated deubiquitination of FASN, increasing FASN stability and lipid synthesis, and accelerating tumor progression. Either orlistat-mediated FASN inhibition or Y043-8015-induced disruption of the CCT2-EIF3F interaction effectively suppressed CCT2-driven tumor progression in vivo. Importantly, combined treatment produced synergistic antitumor effects, significantly reducing tumor growth and metastatic burden across multiple in vivo models, including isograft and patient-derived xenograft models. This study reveals that CCT2 promotes lipid metabolic reprogramming and tumor progression in prostate cancer by cooperating with EIF3F to stabilize FASN, highlighting the CCT2-EIF3F-FASN axis as a potential target for metabolic intervention. - Source: PubMed
Publication date: 2026/06/03
Xu ShunZhang YifanLi HaolinZhao ShengyuDai XiaoranXu QiliFei MintianLi ChunZou ZhihuiWang BaojunZhang LiWang HuiZhang LigangLiang Chaozhao - Prostate cancer (PCa) progression, particularly to castration-resistant prostate cancer (CRPC), is driven by androgen receptor (AR) reactivation and epigenetic alterations. Here, we identify lysine methyltransferase 2D (KMT2D) as a critical epigenetic oncogene in PCa. KMT2D expression is elevated in PCa and correlates with poor prognosis. Mechanistically, KMT2D facilitates AR signaling by recruiting the pioneer factor FOXA1 to AR-specific enhancers, promoting chromatin accessibility and activating AR target genes. FOXA1 mutations impair this regulation, demonstrating their functional interplay. Furthermore, KMT2D-FOXA1-AR axis modulates ketone body metabolism via transcriptional control of HMGCS2, supporting tumor growth. Pharmacological inhibition of UTX, a COMPASS complex demethylase essential for KMT2D function, disrupts H3K4me1 deposition and suppresses AR signaling and tumor proliferation. Altogether, we characterize KMT2D as a key driver of AR-dependent PCa progression and propose UTX inhibition as a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/05/30
Luo MayaoWu ChenweiZhou ManliLiu RuiZhang YifanLi YadongLiao YuanpengHuang XinDu ChuanceLv ShidongWei Qiang