Ask about this productRelated genes to: ARID3A antibody
- Gene:
- ARID3A NIH gene
- Name:
- AT-rich interaction domain 3A
- Previous symbol:
- DRIL1
- Synonyms:
- BRIGHT
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2015-11-17
Related products to: ARID3A antibody
Related articles to: ARID3A antibody
- Ferroptosis, a unique modality of regulated cell death, has become an emerging strategy for tumor therapy. Multiple cellular pathways, including redox homeostasis, iron handling, epigenetic regulation, and metabolic changes, could mediate ferroptosis. Here, we demonstrate that high expression of iron-responsive element binding protein (IRP1)/A + T rich interaction domain protein 3a (ARID3A) inhibits ferroptosis and enhances chemoresistance of pancreatic cancer cells via handling the promoter region of a ferroptosis gene, cytoglobin (CYGB). Mechanistically, the high level of iron leads to nuclear translocation of IRP1 and ARID3A, thereby mediating ARID3A binding to the promoter region of CYGB and down-regulation of chromatin accessibility. The decrease of CYGB expression results in pancreatic cancer cell resistance to ferroptosis, which makes them more resistant to chemotherapy. Clinically, high expression of IRP1 and ARID3A associates with unsatisfactory chemotherapeutic response and poor survival of patients with pancreatic cancer. Our study highlights the role of IRP1/ARID3A complex as a chemotherapy target and its potential in the combined application of ferroptosis drugs. - Source: PubMed
Publication date: 2025/09/24
Li ZeruQin ChengZhao BangboLi TianyuZhao YutongHuang LiruiShi HaoyuXie YipingYan YutongZhang XiangyuWang Weibin - Conventional diagnostic strategies for prostate cancer (PCa) are hindered by suboptimal specificity, frequently resulting in overdiagnosis and unnecessary invasive biopsies. We developed an integrative diagnostic framework based on transcriptomic signatures from tRNA-derived fragments (tRFs), target genes, and lactylation-related genes (LRGs), two emerging regulators linked to PCa progression. - Source: PubMed
Wang LeiHu XiaoxueWang BixiZhang YapingYang JiajiaWang Ying - Immune checkpoint blockade (ICB) shows limited clinical activity in TNBC, largely because immune-cold tumors fail to sustain productive innate and adaptive anti-tumor immunity within an immunosuppressive tumor microenvironment. Here, we identify the transcription factor ARID3A as a tumor-intrinsic regulator of this resistant state. Genetic ablation of ARID3A inflamed the tumor microenvironment, enhanced dendritic-cell activation, increased antigen-specific tetramer-positive and total CD8 T-cell infiltration with heightened cytotoxic activity, and sensitized otherwise resistant tumors to PD-1 blockade in vivo. Mechanistically, ARID3A restrained endogenous nucleic-acid sensing and downstream type I interferon signaling, predominantly through cGAS-STING with a contributory RIG-I-MAVS component. Through structure-guided drug repurposing, we identified the clinically approved migraine agent rimegepant as an ARID3A-targeting small molecule. Direct binding assays, together with binding-pocket mutations (Y326A and R266A) in matched-expression rescue systems, provided strong genetic evidence for on-target engagement of rimegepant with ARID3A. Rimegepant phenocopied ARID3A loss, reactivated innate immune signaling, and markedly enhanced anti-PD-1 efficacy in murine TNBC models and patient-derived organoids. Collectively, our findings define an actionable ARID3A-IFN axis and support clinical evaluation of rimegepant-based immunotherapy combinations, particularly in ARID3A-high, immune-cold TNBC. - Source: PubMed
Publication date: 2026/06/02
Zhou TengZhu YifeiZeng ChengHan JinluHuang HuiyingLi DoudouLin MingxiJin YiziGuo QinYan YuxinMao XinhuiZhou YifeiZhang Jian - Cranial neural crest (CNC) cells are a key stem cell like tissue that contribute to most of the facial structures in vertebrates. A disintegrin and metalloproteinase (ADAM) family of proteins is essential for the induction and migration of the CNC. We have shown that Adam13 interacts with the transcription factor Arid3a to regulate gene expression; we show that Adam13 modulates histone modifications in the CNC and that Arid3a binding to the promoter is dependent on the presence of Adam13. These associations promote the expression of a certain variant expressed in the CNC that uniquely activates the expression of genes critical to CNC migration. Furthermore, we show that both Adam13 and human ADAM9 are associated with proteins involved in histone modifications and RNA splicing (a function critically affected by the loss of Adam13). Thus, we propose that ADAMs may act as extracellular sensors to modulate chromatin availability, leading to changes in gene expression and splicing. - Source: PubMed
Publication date: 2026/05/07
Pandey AnkitCousin HeleneKumar ShivTaylor LouisChander AshmitaCoppenrath KelseyShaidani Nikko-IdeenHorb MarkoAlfandari Dominique - The AT-Rich Interaction Domain (ARID) family plays critical roles in malignancies. Although numerous members have been shown to influence cancer processes, there is a lack of a general understanding of the ARID family in colon cancer. To address this gap, we used bioinformatic technologies to investigate the role of the ARID family as a whole and to identify the crucial member. Subsequently, cell growth assays, transwell assays, and animal models were employed to validate the key member's effect on colon cancer growth and metastasis. Furthermore, bioinformatics and immunohistochemistry were utilised to explore the potential mechanisms and evaluate the efficacy of a targeted intervention strategy. Our results showed that the ARID family was upregulated in colon cancer, with ARID3A being the main component that promoted colon cancer development. Specifically, ARID3A enhanced colon cancer cell proliferation, migration, and invasion both in vivo and in vitro. Mechanistically, this promotional effect could be associated with ARID3A promoting PGE2 synthesis and triggering macrophage infiltration. Notably, aspirin treatment reduced the PGE2 level, which significantly inhibited the malignant behaviour of ARID3A-overexpressing cells. In conclusion, ARID3A was a key member of the ARID family in the development of colon cancer. ARID3A was an underlying biomarker for aspirin administration. - Source: PubMed
Li JiadeLi MuhanLi QuanfuWu YungaowaShen YifanLi YanpingZhang MingshuoWang GuangyouZhu Yuanyuan