Ask about this productRelated genes to: NR2C1 antibody
- Gene:
- NR2C1 NIH gene
- Name:
- nuclear receptor subfamily 2 group C member 1
- Previous symbol:
- TR2
- Synonyms:
- TR2-11
- Chromosome:
- 12q22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-11-09
Related products to: NR2C1 antibody
Related articles to: NR2C1 antibody
- Members of the nuclear receptor subfamily 2, group C (NR2Cs), despite sharing structural homology with established biomarkers like estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR), remain underexplored in breast cancer (BC). This study aims to elucidate the subtype-specific prognostic significance of NR2Cs and investigate the molecular and immunomodulatory mechanisms of NR2C2 in restricting BC progression. We integrated transcriptomic data from TCGA with functional genomics to analyze NR2Cs expression and patient prognosis. Mechanistic landscapes were characterized using pathway enrichment, protein-protein interaction networks, immune infiltration algorithms, and pharmacogenomic drug sensitivity correlation. In vitro validation was performed using cell proliferation, colony formation, 5-Ethynyl-2'-deoxyuridine (EdU), and wound healing assays. In vivo antitumor efficacy and T-cell infiltration levels were evaluated using orthotopic human MDA-MB-231 xenografts in BALB/c nude mice and syngeneic murine EO771 tumors in immunocompetent C57BL/6 mice, supplemented by multiplexed immunohistochemistry. Both NR2C1 and NR2C2 were significantly downregulated in BC tissues compared with normal controls. NR2C2 demonstrated a robust, pan-subtype protective profile, correlating with prolonged survival across major molecular subtypes, particularly in ER-positive cohorts. In silico profiling connected NR2C2 to transforming growth factor-β (TGF-β) pathway inhibition and tumor-immune T-cell infiltration enhancement. In vitro, NR2C2 overexpression significantly suppressed BC cell proliferation, colony formation, DNA synthesis, and migratory capabilities. In vivo, NR2C2 overexpression markedly restricted tumor growth in both models. Mechanistically, this tumor-suppressive effect was characterized by cell-intrinsic growth arrest (decreased Ki-67), induced apoptosis (increased Cleaved Caspase-3), and significant inhibition of the TGF-β pathway (decreased Smad). Concurrently, in the immunocompetent syngeneic model, Nr2c2 overexpression promoted a robust recruitment of infiltrating CD4 and cytotoxic CD8 T cells into the tumor microenvironment. Our findings establish NR2C2 as a pivotal tumor suppressor in BC that restrains tumor progression by attenuating TGF-β signaling, thereby simultaneously suppressing cell-intrinsic proliferation and promoting T-cell infiltration into the tumor microenvironment. This study offers a promising therapeutic paradigm bridging orphan nuclear receptor biology with active cancer immunotherapy. - Source: PubMed
Publication date: 2026/10/03
Li XiaofenYu XiaoqinHuang KaiyanLuo ShipingLi JingSong ChuanguiZhang Jie - Lipid metabolism involves multiple genes that contribute to various diseases including metabolic disorders. Although extensive research has focused on identifying large-effect variants in coding regions, few studies have examined the effects of variations in regulatory and non-coding regions. Apolipoprotein C2 (APOC2) gene plays a central role in activating lipoprotein lipase; however, the effect of upstream variants on its transcriptional regulation remains unclear. We aimed to (1) identify genetic variants in a targeted APOC2 upstream region of, (2) annotate and characterize predicted cis-regulatory elements (CREs) in-silico, (3) map identified variants to transcription factor binding sites (TFBS), and (4) evaluate the association of selected variants with dyslipidemia and body mass index (BMI). - Source: PubMed
Publication date: 2026/07/21
Al-Bustan Suzanne AAnnice Babitha GAlhaddad Hasan - Gastric cancer is a leading cause of cancer-related death, particularly in East Asia, yet its genetic basis remains incompletely understood. Using genome-wide association study data from BioBank Japan, we show that gastric cancer shares significant genetic associations with 25 other phenotypes, most notably cardiovascular conditions such as angina pectoris and myocardial infarction. Mendelian randomization supports a causal role of these traits in gastric cancer risk. Multitrait analysis of GWAS reveals a novel pleiotropic locus at 12q22 (rs12814712) that is shared between gastric cancer and cardiovascular traits. Functional experiments demonstrate that the risk allele at this locus reduces transcriptional activity and downregulates the expression of nearby genes, particularly VEZT. In gastric cancer cells, overexpression of VEZT and NR2C1 suppress proliferation and migration, whereas their knockdown promotes malignancy. Our analysis identifies rs12814712 as a novel susceptibility locus for gastric cancer and underscores its regulatory role in disease-related gene networks. - Source: PubMed
Publication date: 2026/03/15
Ding HuanxinLiu ChuxuanSun QingJiang YueXu QianZhu ZhenguoJin XinHuang QiboLi YueSong YingchaoLiu ZenglinYu TianmingShi BowenTan DelinLi LinzehaoMentch FrankGlessner JosephChang XiaoHakonarson HakonZhang Guangyong - Skeletal muscle development, a precisely orchestrated process, is vital for animal movement, energy metabolism, and meat production. Among Chinese poultry breeds, the Pekin duck and Liancheng duck are prominent, distinguished by their unique meat qualities and growth rates. In this study, we identified developmentally dynamic genes (DDG) by RNA sequencing of skeletal muscle tissues at different time points, from 1 to 42 days after birth, and found DDGs with opposite expression patterns in the early and late periods of skeletal muscle development. The high-to-low (earlyDDGs) and low-to-high (lateDDGs) expressed genes in two duck breeds, which show different functional enrichment features, were potentially regulated by different mutually inhibitory toggle-switch developmentally dynamic transcription factor (DDTF) pairs and alternative splicing. In Pekin ducks, interactions between earlyDDTFs (ZEB1, RORA, E2F6, PLAG1, MSANTD3) and lateDDTFs (ATF4, SIX2, ZBED4) predominantly affect earlyDDGs, prioritizing neuron establishment and optimization and lateDDGs enriched in VEGF-VEGFR2 signaling and cell division. In contrast, in Liancheng ducks, interactions between earlyDDTFs ATF2, FOXP2, NR2C1, GLIS2 and lateDDTFs ESRRB, MYCN are likely to affect earlyDDGs more involved in intracellular coordination and proliferation and lateDDGs involved in aerobic respiration and fatty acid beta-oxidation. Besides, differences in alternative splicing were observed for DDGs such as COL13A1 and RNF10, which may affect neurotransmission and vascular smooth muscle cell proliferation during skeletal muscle development between two duck breeds. These findings enhance our understanding of differences in regulatory mechanisms of skeletal muscle development between Pekin duck and Liancheng duck. - Source: PubMed
Publication date: 2025/08/15
Ding DingbangKinkpe LionelLi YangZhang YunshengWang Xia - The RNA helicase DDX41 is a DEAD-box helicase that is well known as a virus sensor in dendritic cells and a tumor suppressor that is frequently mutated in myeloid neoplasms. However, the functions and relevance of DDX41 in solid tumors remain largely unexplored. In this study, through in vivo CRISPR screening, we demonstrate that DDX41 is highly expressed in various solid tumor types and promotes tumorigenicity in liver cancer. Mechanistically, DDX41 facilitates R-loop processing and accelerates the transcription of RPL/RPS genes, thereby promoting ribosome biogenesis and protein synthesis. Additionally, we show that the acetyltransferase KAT8 is required for H3K9ac modification of the DDX41 promoter and that NR2C1/NR2C2 are responsible for DDX41 expression. Moreover, elevated DDX41 levels increase liver cancer cell sensitivity to protein synthesis inhibitors; treatment with homoharringtonine (HHT), an approved drug, significantly inhibits tumor growth in DDX41-overexpressing liver cancer models. Taken together, the results of this study highlight that DDX41 acts as an oncogene in liver cancer and suggest that protein synthesis inhibition may be a promising therapy for liver cancers with high DDX41 expression. - Source: PubMed
Publication date: 2025/08/11
Li HongquanHe YifeiJiang JiawenLiu ZhenLiu YizheShi QiliDing JieLi HaochenSun WeiliHu XinChen ZhiaoHe Xianghuo