Ask about this productRelated genes to: PTGES3 Blocking Peptide
- Gene:
- PTGES3 NIH gene
- Name:
- prostaglandin E synthase 3
- Previous symbol:
- -
- Synonyms:
- p23, TEBP, cPGES
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-28
- Date modifiied:
- 2016-10-05
Related products to: PTGES3 Blocking Peptide
Related articles to: PTGES3 Blocking Peptide
- Hepatocellular carcinoma (HCC) is characterized by the synchronization of tumor cell proliferation and an immunosuppressive microenvironment. Decoupling these interconnected processes represents a major therapeutic challenge. Although Prostaglandin E Synthase 3 (PTGES3) functions canonically as a cytoplasmic Heat Shock Protein 90 (HSP90) co-chaperone, its non-canonical nuclear role in orchestrating tumor-immune crosstalk remains undefined. Here, we identify PTGES3 as a dual-function regulator coupling tumor intrinsic growth with extrinsic immune remodeling. We report that PTGES3 is upregulated in HCC and serves as an independent prognostic factor for poor survival. Using an immunocompetent, diethylnitrosamine (DEN)-induced HCC mouse model, we demonstrate that hepatocyte-specific Ptges3 silencing significantly suppresses tumorigenesis. Single-cell RNA sequencing (scRNA-seq) and histological analysis reveal that PTGES3 deficiency remodels the immune landscape, specifically by impairing tumor-associated macrophage (TAM) infiltration and M2 polarization. Mechanistically, we identified a specific G-rich motif on the Specificity Protein 1 (SP1) promoter bound by PTGES3 (confirmed via electrophoretic mobility shift assay [EMSA] and Cleavage Under Targets and Tagmentation [CUT&Tag]), which drives SP1-mediated Transforming Growth Factor-β (TGF-β) secretion. This axis appears to exert dual oncogenic effects: triggering paracrine M2 macrophage polarization to foster immunosuppression, whilst simultaneously fueling an autocrine TGF-β/TGFBR/PI3K/AKT/mTOR signaling loop to sustain tumor proliferation. Our findings define a non-canonical nuclear function for PTGES3, identifying it as a critical molecular switch that couples tumor aggressiveness with microenvironmental remodeling, thus presenting a promising therapeutic target for HCC. - Source: PubMed
Publication date: 2026/03/25
Wang NianfeiChen WeiShen ShuminQi JianWang ShanghuWang RongLi MingChen ZixiangChen JiangmingHong BoWang Hongzhi - Damp-heat gout (DHG) is a highly certified type of disease integrated with syndrome in TCM. The ambiguity of its pathomechanism and the lack of quantifiable indicators limit its clinical accurate diagnosis and treatment. This study aimed to elucidate the pathological mechanism of DHG and establish a symptom-centered diagnostic and therapeutic model. We recruited 136 participants, comprising healthy controls (HCs) and DHG patients. Serum metabolomics and proteomics analyses were performed to screen common pathways. Based on the biological significance of these common pathways, a symptom-pathway correlation network was constructed to clarify the pathological mechanisms driving DHG occurrence and progression. Enrichment scores and correlations with key DHG symptoms were used to identify critical pathways. Differential metabolites and proteins associated with these critical pathways served to establish a multi-index diagnostic model and identify potential therapeutic protein targets. Integrated metabolomic and proteomic analyses revealed 21 common pathways associated with DHG. Four crucial pathways, such as Bile secretion, Cholesterol metabolism, Purine metabolism, Arachidonic acid metabolism, were exhibited significant correlations with core DHG symptoms. Furthermore, six pathway-related biomarkers were identified: Hypoxanthine, Prostaglandin E2, Uric acid, Deoxycholic acid, Taurochenodeoxycholic acid, and Bilirubin. The combined diagnostic efficacy of these biomarkers was optimal (discovery cohort: AUC = 0.987; validation cohort: AUC = 0.997). Six protein targets were identified from the crucial pathways, including ATP1A1, APRT, ANGPTL4, GLUT1, PTGES3 and LIPA. This study establishes a symptom-centered diagnostic and therapeutic model for DHG utilizing the identified biomarkers and clarifies the involvement of critical metabolic pathways in DHG pathogenesis, providing novel targets for improved clinical diagnosis and therapy. - Source: PubMed
Publication date: 2026/02/06
Yang LeSun YeLi ChuanningSun HuiWei ShuyunZhu FangjieWang WenkaiHuang RunyueSun XinWang MaojieYan GuangliWang Xijun - The ATP-binding cassette subfamily C member 1 (ABCC1) is a key efflux pump that contributes to multidrug resistance in cancer by exporting chemotherapeutic agents and xenobiotics. Although ABCC1 is clinically important, the phosphorylation-dependent regulatory mechanisms governing its activity remain poorly understood, representing a major knowledge gap. To address this gap, we performed a large-scale integrative analysis of publicly available phosphoproteomic datasets curated from over 3800 PubMed-indexed studies. From 688 high-confidence datasets, we mapped Class I phosphosites on ABCC1 and focused on two predominant sites, S919 and S930, located within the cytoplasmic linker domain. Using phosphosite co-occurrence and co-regulation strategies, we identified phosphorylation events that consistently co-regulate with these key ABCC1 sites across diverse experimental conditions. Through multilevel statistical filtering (Fisher's exact test, < 0.05), recurrence analysis, and experimental context diversity, we defined a high-confidence co-regulatory network comprising 1266 phosphosites across diverse proteins. Mechanistically, this network reveals coordinated phosphorylation of ABCC1 with its known interacting partners, including PTGES3, FASN, and STX4, as well as functionally associated drug transport proteins such as ABCC4, SLC16A1, and SLC20A2. Functional enrichment analysis further linked the ABCC1-centred phospho-network to carcinogenesis, cell-cycle regulation, and drug resistance pathways, highlighting its systems-level role in cancer biology. From a translational perspective, our findings identify phosphosites within the ABCC1 linker domain as actionable regulatory nodes that may be exploited to modulate transporter function, offering potential strategies to overcome chemoresistance. - Source: PubMed
Publication date: 2026/02/16
Nandakumar RevathyMahin AlthafGopalakrishnan Athira PerunellySubair SuhailKrishnan DeepakRaju Rajesh - Human immunodeficiency virus (HIV) and (Mtb) co-infection remains a major cause of mortality in AIDS patients, yet the mechanisms of pathogen interplay and host immune remodeling remain poorly understood. - Source: PubMed
Publication date: 2025/11/28
Zhao ZihuiHuang SuyueHuang WeiSong WeiLiu LiChen JunZhang RenfangShen Yinzhong - Esophageal cancer (EC) is a common malignancy with poor prognosis. Telomeres, composed of repetitive DNA sequences and shelterin complexes, play important roles in tumor biology. However, the prognostic value of telomere-related genes (TRGs) in EC remains unclear. - Source: PubMed
Publication date: 2025/12/03
Li ShuangFang ChenTao ZhengJiang WeiZhu JingfengYu XiaojunMa Haitao