FOXO3
- Known as:
- FOXO3
- Catalog number:
- 000062A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FOXO3
Related genes to: FOXO3
- Gene:
- FOXO3 NIH gene
- Name:
- forkhead box O3
- Previous symbol:
- FKHRL1, FOXO3A
- Synonyms:
- AF6q21, FOXO2
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-23
- Date modifiied:
- 2015-08-25
Related products to: FOXO3
Related articles to: FOXO3
- Extranodal natural killer/T-cell lymphoma (ENKTL) is clinically characterized by destructive lesions that first appear in the nasal cavity and progress along the midline of the face. It was historically described as "rhinitis gangrenosa progressiva" or "lethal midline granuloma" due to its destructive clinical nature and had significant diagnostic and therapeutic challenges. This review synthesizes about 40 years of research, beginning with the 1980s and 1990s, when the disease was identified as a T-cell- or NK-cell-derived lymphoma, and the authors' discovery that clearly linked it to Epstein-Barr virus (EBV). ENKTL is highly prevalent in East Asia and characterized by a type II EBV latency pattern, in which the oncoprotein latent membrane protein 1 (LMP1) acts as a central driver of pathogenesis, activating critical signaling pathways including JAK/STAT, NF-κB, PI3K/Akt, and RAS/MAPK. These pathways, often bolstered by mutations in genes, trigger an oncogenic cascade involving epigenetic modifiers-enhancer of zeste homolog 2 (EZH2), histone deacetylase (HDAC). The deletion of chromosome 6q, leading to loss of function of tumor suppressor PR domain zinc finger protein 1 (PRDM1) and forkhead box O3 (FOXO3), as well as transcription of TNF α-induced protein 3 (TNFAIP3) and protein tyrosine phosphatase receptor type kappa (PTPRK), also contributes to pathogenesis. In vitro studies by the author's group demonstrated that autocrine/paracrine positive feedback loops involving several pro-proliferative molecules/cytokine/chemokine-CD27, ICAM1, hepatocyte growth factor (HGF), IL-9, IL-10, IL-15, CCL17, CCL22, CXCL10- further amplify ENKTL proliferation. Diagnostic precision has improved through the use of serum EBV DNA copy numbers and viral microRNAs (miRs), specifically miR-BART2-5p, alongside the emergence of soluble CD27 as a novel biomarker. While early anthracycline-based regimens failed due to multidrug resistance (MDR), modern concurrent chemoradiotherapy composed of MDR-independent drugs has significantly improved 5-year overall survival (OS) rates for localized disease to over 80%. For advanced or relapsed/refractory cases, L-asparaginase-based regimens are standard, though outcomes remain unsatisfactory. The therapeutic paradigm is currently shifting toward chemoradiotherapy combined with either immune checkpoint inhibitors or small-molecule drugs. Future research should focus on novel molecular-targeted therapies, immunotherapies, or combination strategies targeting proliferation-related molecules or LMP1. - Source: PubMed
Publication date: 2026/04/17
Harabuchi Yasuaki - Mitochondrial dysfunction and defective mitophagy are closely associated with cancer progression. Forkhead box O3 (FOXO3), a key transcription factor, promotes autophagy by activating autophagy-related genes. Polyphyllin VI (PPVI), a Paris polyphylla-derived steroidal saponin, displays potent antitumor activity. - Source: PubMed
Publication date: 2026/04/06
Zhan XiangrongZhong YifanLiu XuewenPeng WenkangZhang XuXiang KeYu QingqingChai YantingChen YingliLiu YingSi Yuan - To explore the regulatory aspects of mRNAs and miRNAs in suicide, we integrated transcriptomic data from GEO datasets. The analysis of mRNA expression in the prefrontal cortex of suicide victims with major depressive disorder revealed a differential profile with 27 downregulated mRNAs, including , , , , and , which are involved in proteostasis, transcriptional regulation, and apoptosis. Functional enrichment analysis using KEGG and Gene Ontology (GO) revealed significant associations with synaptic plasticity, neuronal survival, and signaling pathways, including MAPK, TGF-β, Wnt, p53, and neurotrophins. Subsequently, using the GSE34120 GEO dataset of miRNAs from the frontal cortex of suicide victims, 105 dysregulated miRNAs were identified. The networks revealed compact regulatory modules with hsa-miR-576-3p, hsa-miR-493, and hsa-miR-550, as well as highly connected central nodes such as hsa-miR-30b, hsa-miR-16a-5p, hsa-miR-181a-5p, and hsa-miR-184. The integration of both profiles allowed the elaboration of miRNA-mRNA regulatory networks in which , , , and interact with multiple dysregulated miRNAs. These findings support the notion that suicide involves complex post-transcriptional dysregulation, particularly related to astrocytic function and neurotrophic signaling, with potential diagnostic and therapeutic applications. - Source: PubMed
Publication date: 2026/03/30
Cortéz-Sánchez José LuisRivera-Escobar Hernán MauricioMuñoz Roa Esther NataliaZabala-Bello Carlos AndrésPérez-Sánchez GilbertoChin Chan José MiguelBautista-Ortiz MonserratLópez-Martínez Karla MaríaOsorio-Antonio FedericoGálvez-Romero José LuisCarrasco Carballo AlanSedeño-Monge VirginiaCastelán FranciscoBautista-Rodríguez Elizabeth - Metabolic reprogramming is a hallmark of tumorigenesis and progression in hepatocellular carcinoma (HCC) and has emerged as a promising therapeutic strategy. Forkhead box O3 (FOXO3), a critical nuclear transcription factor, is dysregulated in multiple cancers; however, its precise role in HCC progression remains unclear. In this study, we demonstrate that enhanced glycolysis and glutaminolysis are pivotal metabolic features of HCC, with tumor cells heavily relying on both pathways for survival and proliferation. We identify FOXO3 as a tumor suppressor in HCC that inhibits key metabolic enzymes and metabolites involved in these pathways. This inhibitory effect is mediated through suppression of yes-associated protein (YAP). Mechanistically, FOXO3 directly binds to the GTGAACAT motif (-1824 to -1817) within the YAP promoter, leading to transcription repression of YAP and subsequent disruption of YAP-driven metabolic programs. Pharmacological activation of FOXO3 using specific inducers markedly reduced YAP expression, resulting in inhibition of glycolysis, glutaminolysis, and proliferation in HCC cells. In vivo, activation of the FOXO3/YAP axis effectively suppressed HCC progression through the coordinated inhibition of glycolysis and glutaminolysis. Moreover, FOXO3 inducers significantly impaired the growth and viability of patient-derived HCC organoid models. Hence, these findings identify FOXO3 as a key regulator of metabolic reprogramming in HCC and establish the FOXO3/YAP axis as a promising therapeutic target, suggesting potential strategies for metabolic-based interventions in HCC treatment. - Source: PubMed
Publication date: 2026/04/13
Wang FanHuang MengSheng KaixuanYan YueZhang BeibeiWang XinleiYang ZhiyiLi MengyiLiu YupingQi QiSun YuejunLi Chenglin - Periodontitis is a prevalent oral disease characterised by chronic inflammation and irreversible alveolar bone loss. Osteoclasts (OCs) are the key cells mediating bone resorption and their excessive formation disrupts bone homeostasis. Since apoptosis of OCs normally restrains this process, its failure can sustain bone loss. However, its role in periodontitis remains unclear. Analysis of single-cell RNA sequencing (scRNA-seq) data retrieved from the Gene Expression Omnibus (GEO) database revealed impaired OC apoptosis in the periodontal tissues of individuals suffering from periodontitis. Notably, we observed a reduction in cytoskeleton-associated protein 4 (CKAP4) expression correlating with decreased OC apoptosis. Further investigations using Ckap4 knockout mice confirmed that CKAP4 promotes OC apoptosis through the activation of forkhead box O3 (FOXO3)-induced endoplasmic reticulum stress (ERS). CKAP4 regulates OC apoptosis to maintain periodontal homeostasis and its downregulation in periodontitis promotes pathological bone resorption. This study elucidates CKAP4-mediated apoptotic pathways in OCs, providing mechanistic insight and potential therapeutic strategies to restore OC balance and prevent bone loss. - Source: PubMed
Publication date: 2026/04/13
Cheng JiayuTao DihaoWang WenzheWang HuiyuWang HanzheLiang YufanGuo JiaLiu WenhaoWang YimingYang JianhuaHe XiaoningShan CeLi Bei