PTGES Antibody (N-term)
- Known as:
- PTGES Antibody (N-terminus)
- Catalog number:
- AP8589a-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- PTGES Antibody (N-term)
Related genes to: PTGES Antibody (N-term)
- Gene:
- PTGES NIH gene
- Name:
- prostaglandin E synthase
- Previous symbol:
- MGST1L1
- Synonyms:
- MGST-IV, PIG12, MGST1-L1, TP53I12
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-10-05
Related products to: PTGES Antibody (N-term)
Related articles to: PTGES Antibody (N-term)
- Colorectal cancer (CRC) is one of the global health issues. Current treatments still present major challenges such as off-target cytotoxicity and the emergence of drug resistance, the development of potent and innovative therapeutics is urgently needed. Here, we synthesized copper‑aluminum (CuAl) layered double hydroxides (LDH) using a hydrothermal method and loaded them with the 5-fluorouracil (5-FU) (CuAl-5FU) to improve their anticancer efficacy. The LDHs were 2D-sheeted and rosette-like in shape. The hydrodynamic diameter of CuAl and CuAl-5FU was 568 and 661 nm, respectively. Zeta potential values of CuAl-5FU ranged from +31.39 to +34.93 mV across pH 3 to 9, indicating good colloidal stability. The drug loading and encapsulation efficiency were 18.19% and 36.37%, respectively. Dose-dependent cytotoxicity was seen in HCT-116 and HT-29 CRC cells. Comparatively, CuAl-5FU LDH exhibited greater anticancer activity compared to LDH alone and free 5-FU drug in both monolayer and tumor spheroid models. Mechanistic studies revealed that CuAl-5FU significantly induced reactive oxygen species (ROS) production, mitochondrial membrane depolarization, and promoted apoptosis by upregulating the pro-apoptotic Bax protein and PARP cleavage in both CRC cells. Transcriptomic analysis and qPCR validation revealed the downregulation of oncogenic MAPK signaling and modulation of key genes related to proliferation (JUN, DUSP1, FOSB, EGR1, and FOS), apoptosis (TP53I3, ZMAT3, GADD45A, BBC3, MDM2, TNFRSF10B, E2F1, and ORC1), and cell cycle arrest (CDKN1A and CDC25A). Notably, we identified altered expression of several chemoresistance-related genes (AVPI1, HROB, DDIAS, PTGES, and LAMA3), suggesting the early emergence of adaptive responses in CRC cells. To validate this observation, CuAl-5FU-resistant HCT-116 G3 and HT-29 G2 cell lines were established and their chemoresistant phenotypes were characterized. Indeed, the chemoresistance-associated genes were upregulated, together with significantly higher IC values and clonogenic survival fractions than their respective parental cells. Collectively, these findings suggest that CuAl-5FU improves anticancer activity in CRC cells by modulating multiple genes involved in ROS production, mitochondrial membrane depolarization, apoptosis, and cell cycle regulation. Nevertheless, chemoresistance developed rapidly following repeated treatment, highlighting a potential limitation of this therapeutic approach. Overall, this study provides a new potential strategy for CRC treatment while emphasizing the importance of elucidating the molecular mechanisms underlying acquired chemoresistance. Future studies should also optimize the physicochemical properties of the CuAl-5FU LDH, particularly the large particle size (∼661 nm) by optimizing the hydrothermal synthesis conditions and incorporating surface modifications to further improve the tumor penetration and drug delivery. - Source: PubMed
Publication date: 2026/07/10
Yin YingShi JiayanLu DingyiWang YueranXiang XuemianLiu RuohanHu ZhantuBahadur AliArtoadi Muhammad IdrusZheng ChenxiaoShameli KamyarZhang XiaodongTeow Sin-Yeang - The bladder is highly susceptible to chemical carcinogens rendering bladder cancer one of the most prevalent cancers globally. While microsomal prostaglandin E synthase-1 (mPGES-1) is known to promote carcinogenesis in several tissues such as the colon and skin, its involvement in bladder cancer has not been fully investigated. This study aimed to clarify whether mPGES-1 promotes chemically-induced bladder carcinogenesis using a gene-deficient mouse model and evaluate its potential as a novel therapeutic target. - Source: PubMed
Sasaki YukaEndo YukiOchiai TsubasaKin MasaokiSuzuki YasutomoKondo YukihiroHara Shuntaro - Ovarian cancer shows limited responsiveness to immune checkpoint blockade, suggesting that malignant cells harbor intrinsic programs capable of suppressing T cell-mediated antitumor immunity. To uncover these programs under fixed recognition signal conditions, the research team established and optimized a B7H3×CD3-based, MHC-independent redirected cytotoxicity platform, which generated a reproducible partial-killing window. By screening 1796 bioactive compounds in paired SKOV3 monocultures and SKOV3/PBMC co-cultures, the researchers distinguished immune-sensitizing perturbations from direct cytotoxic agents and identified I-BRD9, a selective BRD9 bromodomain inhibitor, as a top candidate. I-BRD9 enhanced T cell-mediated killing in ovarian cancer models, B7-H3-positive benchmark cell lines, and patient-derived ovarian tumor suspensions, without affecting tumor cell or PBMC viability. Cross-cell line RNA-seq analysis revealed that BRD9 inhibition reshapes a coordinated immune resistance program involving PGE2 biosynthesis, inhibitory ligands, T cell-attracting chemokines, antigen presentation-related transcripts, and extracellular matrix features. Within this program, siRNA-mediated PTGES knockdown functionally recapitulated key effects of I-BRD9 by restoring chemokine/PGE2-axis transcripts, promoting CD8 T-cell proliferation and IFN-γ production, and enhancing T-cell effector-associated gene expression. These findings establish the BRD9-PTGES/PGE2 axis as an actionable tumor-intrinsic pathway that limits ovarian cancer sensitivity to T cell-mediated cytotoxicity. - Source: PubMed
Publication date: 2026/06/23
Guo ShanniShi PengYang ChangruiQian ShuyiYang FanYin XiaSun Bowen - Cerebral malaria (CM) is a life-threatening neurological complication of infection characterized by excessive inflammation, blood-brain barrier (BBB) disruption, and immune dysregulation. Macrophage-mediated inflammatory responses play a central role in CM pathogenesis, where imbalanced activation contributes to disease progression and tissue damage. However, integrated analyses combining macrophage surface phenotyping with transcriptional profiling remain limited, restricting comprehensive understanding of immune modulation during CM. - Source: PubMed
Publication date: 2026/06/10
Gupta AartiSharan Thakur RevaOjha Rajesh KumarKhan TahseenKalkal MeenuDas Jyoti - Uncontrolled hemorrhage in trauma, surgical, organ-related, and endoscopic settings, particularly in patients receiving antiplatelet therapy, remains difficult to manage clinically. Here, we introduce a high phosphatidylserine (PS)-exposed procoagulant platelet (hPPL) derivative reprogrammed from isolated platelets via calcium ionophore A23187-induced apoptosis, enriched in surface PS and capable of driving rapid hemostasis. Retaining a protein profile akin to resting platelets, hPPLs robustly promoted platelet activation and aggregation in human- and rat-derived plasma and whole blood in vitro and demonstrated superior hemostatic efficacy compared with clinical thrombin and commercial hemostatic materials [microporous polysaccharide hemispheres (MPH) and FIBRILLAR] in murine liver injury and porcine gastric ulcer bleeding models, even under antiplatelet treatment. Mechanistically, hPPLs up-regulated prostaglandin E synthase (PTGES), thereby increasing prostaglandin E2 (PGE) production and its receptor 3 (EP3)-mediated platelet activation, which reinforced PS-mediated clot formation. Our findings identified an apoptosis-driven PTGES-PGE-EP3 signaling axis that augmented PS-mediated coagulation in murine and porcine hemorrhage models and established the hPPL derivative as a topical hemostatic agent with translational potential for organ-related bleeding and distinct advantages in managing complex endoscopic hemorrhages under both physiological and coagulopathic conditions. - Source: PubMed
Publication date: 2026/06/03
Wang PeinaDu ShuailunWu SuyingZhai YaqiBai JiaweiSafdar AmmaraLiu ZhenyuLu ZefangLi BozhaoCheng JinSong YuchangZhang RuiLi DandanWang ZhichengZeng ZexianNie GuangjunChang Yan-ZhongLi Suping