Ask about this productRelated genes to: NR3C2 Blocking Peptide
- Gene:
- NR3C2 NIH gene
- Name:
- nuclear receptor subfamily 3 group C member 2
- Previous symbol:
- MLR
- Synonyms:
- MR
- Chromosome:
- 4q31
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-19
- Date modifiied:
- 2015-11-18
Related products to: NR3C2 Blocking Peptide
Related articles to: NR3C2 Blocking Peptide
- Ovarian cancer (OV) is among the most lethal forms of gynecological cancers. This work aims to investigate the roles and underlying mechanisms of Tanshinone IIA (Tan IIA) in the epithelial-to-mesenchymal transition (EMT) process in OV. Tan IIA inhibited OV cell proliferation, migration, invasion, and EMT in a dose-dependent manner. Knockdown of nuclear receptor subfamily 3 group C member 2 () weakened the efficacy of Tan IIA, while combined overexpression of inhibitor of growth protein 1 () rescued the OV progression promoted by NR3C2 knockdown. NR3C2 occupied the ING1 promoter to exert transcriptional activation. Patients with low NR3C2/ING1 expression were associated with more advanced FIGO staging, larger ascites volume, and peritoneal metastasis, and had significantly poorer survival outcomes. Collectively, Tan IIA upregulates NR3C2 expression and activates ING1 transcription to exert its anti-metastatic effects by inhibiting EMT in OV. The study also underscored the prognostic potential of NR3C2/ING1 for OV. - Source: PubMed
Publication date: 2026/04/30
Wang XiaoqinZhang DuoyiWang TingtingLi XinZhang Jing - Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon from tobacco smoke, exhaust, and pollutants, is linked to bladder cancer (BLCA). We systematically analyzed GEO datasets to identify BaP-related differentially expressed genes (DEBRGs). By integrating network toxicology, machine learning, molecular docking, molecular dynamics, and single-cell transcriptomics, we identified 19 significant genes, among which 7 key DEBRGs were prioritized (GSK3B, SKP2, AURKB, EPHB4, KIT, NR3C2, and CA2) in BaP-mediated BLCA. SHAP analysis highlighted GSK3B and SKP2 as important genes contributing to the predictive model. Single-cell data revealed their cell-type specific expression in the tumor microenvironment. Molecular simulations detailed interactions between BaP and target proteins. This study identified critical genes in BaP-induced bladder carcinogenesis, offering insights into underlying molecular mechanisms and potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/21
Zhao XinzhaoQin RuizeShen ChengquanHu DingLi ChengLiu ChangxueGe HuaixiWang Yonghua - Gastric cancer (GC) is a major global health challenge. This study explores the efficacy of linalool in GC and further elucidates its underlying mechanisms. Linalool inhibited the proliferation, migration, and invasion of GC cells and prevented transplanted tumor growth in nude mice. Linalool directly interacted with and stabilized the NR3C2 protein, inhibiting its proteasomal degradation. Functional rescue experiments demonstrated that knockdown of NR3C2 partially reversed the antitumor effects of linalool. Further studies revealed that NR3C2 transcriptionally activated NFKBIZ and inhibited NF-κB signaling, and restoring NFKBIZ expression reversed GC progression caused by NR3C2 deficiency. In clinical samples, the expression levels of NR3C2 and NFKBIZ were lower in GC tissues than in adjacent normal tissues, and the two markers were positively correlated in the tumor tissues. Furthermore, low expression of both NR3C2 and NFKBIZ was significantly associated with higher T stages and more advanced pTNM stages and was accompanied by NF-κB signaling activation and elevated levels of inflammatory cytokines in tumor tissues. Overall, linalool inhibits GC progression by upregulating NR3C2 and transcriptionally activating NFKBIZ, thereby suppressing NF-κB signaling. Low NR3C2/NFKBIZ expression is associated with adverse clinical and pathological features in GC. - Source: PubMed
Publication date: 2026/05/18
Hu YingChen ShunfengWang YuLiu LingZhang ChaoyiChen HongDuanmu YuanyuanSu ZhaotianMa Jun - Pseudohypoaldosteronism type I (PHA I) is a rare hereditary disorder of mineralocorticoid resistance, with the renal form predominantly caused by variants. We report a male neonate presenting with severe hyperbilirubinaemia who was subsequently diagnosed with renal PHA I. Born at 38⁺⁶ weeks, he was admitted on day 7 for jaundice. Laboratory evaluation revealed refractory hyponatraemia, markedly elevated plasma aldosterone and renin levels, and ineffective conventional electrolyte therapy. Whole-exome sequencing identified a heterozygous nonsense variant, c.1954C>T (p.Arg652*), in , confirming the diagnosis. Aggressive sodium supplementation corrected the electrolyte imbalance, and follow-up showed normal growth and stable serum sodium. This case underscores the need to consider inherited renal tubulopathies in neonates with refractory hyponatraemia and highlights the pivotal role of genetic testing in precise diagnosis. - Source: PubMed
Publication date: 2026/04/30
Ma HongcaiHan HuijiaoLiu YanyanAn Yong - Oncogenic cell signaling, including the activation of cellular stress or cytokine-induced pathways, is a hallmark of cancer. In triple-negative breast cancer (TNBC), p38 MAPK phosphorylates glucocorticoid receptors (GR) at Ser134 in response to cytokines such as TGFβ1. This activated Phospho-Ser134-GR (pSer134-GR) regulates genes promoting cancer cell migration, invasion, and altered metabolism. Glucocorticoids also activate the functionally and structurally-related mineralocorticoid receptors (MR) whose ligand, aldosterone, mediates hypertension, inflammation and fibrosis. We and others have previously shown the role of GR in the advanced phenotypes exhibited by TNBC, but the potential importance of GR-MR crosstalk and the specific contribution of MR remains unknown. Interestingly, our new analyses of MR expression in TNBC tumors revealed elevated MR transcript levels relative to luminal breast cancer subtypes, which are predictive of worse overall survival. Cytoplasmic MR-GR complexes that are formed upon treatment of TNBC cells with TGFβ1 required both p38 MAPK signaling and pSer134-GR. In contrast, nuclear MR-GR complexes predominated in response to dexamethasone and/or aldosterone. MR antagonists (spironolactone, finerenone) significantly reduced aldosterone- or TGFβ1-induced migratory and stemness properties and blocked MR-pGR and MR-GR interactions; MR knockdown similarly attenuated these advanced cancer phenotypes. MR expression was essential for both a functional p38 MAPK module and pSer134-GR downstream of TGFβ1 receptor activation. Crucially, MR-deficient models exhibited reduced lung metastasis following mouse tail-vein injection, phenocopying cells harboring phospho-mutant S134A-GR. As with p-Ser134-GR, we define a novel role for MR-GR cooperation downstream of TGFβ1 for regulation of TNBC cell migration, stemness, and in vivo lung colonization. - Source: PubMed
Posani Sai HarshitaDiep Caroline HKrutilina Raisa IPlaya Hilaire CSeagroves Tiffany NBlenis JohnLange Carol A