EZH2 Assay Kit
- Known as:
- EZH2 Assay Kit
- Catalog number:
- 52009L
- Product Quantity:
- 100 reactions
- Category:
- Peptides
- Supplier:
- BPS Bioscience
- Gene target:
- EZH2 Assay Kit
Related genes to: EZH2 Assay Kit
- Gene:
- EZH2 NIH gene
- Name:
- enhancer of zeste 2 polycomb repressive complex 2 subunit
- Previous symbol:
- -
- Synonyms:
- EZH1, ENX-1, KMT6, KMT6A
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-21
- Date modifiied:
- 2019-04-23
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- The resistance of human epidermal growth factor receptor 2 (HER2)-positive breast cancer (BC) patients to trastuzumab (Tmab) severely restricts its efficacy. As a natural metabolite with antitumor activity, whether cycloastragenol (CAG) can overcome Tmab resistance and its related mechanism are not clear. This study aims to verify if CAG reverses Tmab resistance in HER2-positive breast cancer cells, clarify its regulatory effects on resistant cell behaviors, and explore the role of the EZH2/PTEN/AKT axis. The study design is combined in vivo and in vitro study. The BT474-TR cells were constructed, and HER2 expression was detected by Western blot and immunofluorescence. Cell Counting Kit-8 assay served to screen the optimal CAG concentration and Tmab dosage. Cell proliferation, migration, and invasion capabilities were evaluated via CFSE staining, colony formation assay, and Transwell and scratch assays. Flow cytometry was employed to examine apoptosis and cell cycle arrest. A xenograft tumor model was established in nude mice. Pathological changes were observed via HE staining, apoptosis was detected using TUNEL staining, microvascular density and VEGF levels were assessed by immunohistochemistry, and protein expression was validated by Western blot. Tmab reduced BT474-TS cell viability and downregulated HER2, while exhibiting minimal effects on HER2-high expression BT474-TR and JIMT-1 cells. CAG treatment enhanced the efficacy of Tmab against drug-resistant cells, reducing cell viability and proliferation, promoting apoptosis, and inducing G0/G1 phase cycle arrest. CAG suppressed migration and invasion capabilities while reversing the EMT phenotype. Additionally, CAG downregulated EZH2 and p-AKT while upregulating PTEN; overexpression EZH2 diminished CAG's antitumor activity. Following CAG combined with Tmab treatment, tumor volume and weight in nude mice were smaller, and tumor tissue exhibited increased pathological damage, elevated apoptotic cells, and reduced microvascular density and VEGF levels. CAG modulates the cell cycle and EMT through the EZH2/PTEN/AKT pathway, effectively overcoming Tmab resistance in HER2-positive BC cells. Clinical trial number: Not applicable. - Source: PubMed
Publication date: 2026/07/27
Wu MingyuanHou FenggangYang ZhaoshuoZhu ZhenfengWang YaoWang Hong - Prostate cancer (PCa) is among the highest incidence malignancies in men, with high rates of inevitable resistance development, relapse, and mortality. Castration-resistant prostate cancer (CRPC) continued to pose substantial therapeutic challenges, highlighting the urgent need for effective treatment options. This study assessed the marine cembranoid sarcophine activity against the progression and recurrence of the metastatic CRPC (mCRPC) in mouse xenograft models. Protein and phosphorylation levels were assessed by immunoblotting and mRNA expression by qPCR and RNA sequencing. The in vivo efficacy was evaluated through tumor progression over 3 weeks followed by primary tumor excision and recurrence monitoring over an 8-week course. Sarcophine significantly reduced the mCRPC CWR-R1ca tumor volume by 74.1% and suppressed the epigenetic regulators EZH2 and SMYD2; lineage plasticity factors ASCL1 and BRN2; Wnt/stemness signaling markers β-catenin and LGR6; AKT total expression and activation; and invasion-associated proteins TRPC4 and MMP2 in primary tumors. Sarcophine effectively prevented the mCRPC locoregional recurrence, as well as lung and spleen distant recurrences, and effectively reduced recurrence in other organs. Transcriptomics-RNA-Seq analysis of primary tumors identified 2697 downregulated and 3534 upregulated genes, indicating broad transcriptional reprogramming following sarcophine treatments. These findings demonstrate coordinated suppression of multi-oncogenic pathways and validate the therapeutic potential of sarcophine to control mCRPC. - Source: PubMed
Publication date: 2026/06/23
Alhowiriny Abdullah TEbrahim Hassan YMudhish Ethar ADawud DalalEl Sayed Khalid A - No effective clinical therapeutic strategies are currently available for paraquat (PQ)-induced pulmonary fibrosis. This study determined whether metformin (MET) ameliorates PQ-induced pulmonary fibrosis and the epithelial-mesenchymal transition (EMT) in alveolar epithelial cells and explored the underlying molecular mechanisms. Expression of EMT-related markers, ferroptosis-related indicators, and caveolin-1 were examined and the regulatory role of the EZH2/H3K27me3 axis was evaluated using in vitro and in vivo models. PQ induced the EMT and ferroptosis in MLE-12 cells. MET upregulated caveolin-1 expression by inhibiting EZH2 and reducing H3K27me3, which in turn suppressed ferroptosis. MET attenuated PQ-induced pulmonary fibrosis via this signaling pathway and these results were further validated in animal models. - Source: PubMed
Publication date: 2026/07/25
Wang LuanMa ZhiyuLi Tiegang - Ligand-mediated targeting of prostate-specific membrane antigen (PSMA) is a prominent strategy in prostate cancer (PCa) theranostics. However, the conventional mechanism of PSMA-targeted nanomedicines, based on passive enhanced permeability and retention (EPR) from leaky vasculature followed by active receptor-mediated uptake, has been challenged by emerging evidence of direct endothelial transport. Here, we developed a PSMA-targeted silicasome (tSil) via peptide modification, which achieved markedly enhanced tumor accumulation compared with non-targeting control in subcutaneous, orthotopic, and bone metastatic PCa models. The ultrastructural transmission electron microscopy and in vivo competitive blocking assays revealed that, in non-leaky vasculature settings where the EPR effect is limited, tSil utilized both non-receptor and PSMA-dependent active transcytosis to traverse endothelial cells and penetrate tumor parenchyma with improved cellular uptake efficiency. To explore the therapeutic potential of this active targeting in metastatic castration-resistant prostate cancer (mCRPC), we co-encapsulated the PARP inhibitor rucaparib and EZH2 inhibitor tazemetostat in tSil to synergistically induce DNA damage and apoptosis. In both subcutaneous and orthotopic models, the tSil platform exhibited superior antitumor efficacy relative to non-targeting formulation. Co-delivery of the PARP/EZH2 inhibitors also upregulated PD-L1 expression and enhanced cytotoxic T cell infiltration, prompting combination with immune checkpoint blockade, which yielded improved outcomes in orthotopic and challenging bone metastasis mouse models. Collectively, this work presents a promising therapeutic strategy for PCa and offers insights into the design of ligand-mediated nanomedicines for efficient tumor drug delivery. - Source: PubMed
Publication date: 2026/07/20
Huang QiangLi YutingBi YifanZhang JiaJiang WeiWang HaoyangZhao JunYang HonghongShi XiayuJiang JinhongYang FeiyaLiu XiangshengZhang Mo - Epigenetic regulation is intimately linked to cellular metabolism, enabling environmental and nutritional cues to shape gene expression programs through dynamic modifications of chromatin structure. This metabolism-epigenetics interface is mediated, in part, by the dependence of chromatin-modifying enzymes on key metabolites, including S-adenosylmethionine (SAM), acetyl-CoA, UDP-GlcNAc, and α-ketoglutarate, which serve as substrates or cofactors for DNA and histone modifications. Among these regulators, EZH2, the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), has emerged as a key mediator linking metabolic state to epigenetic regulation by translating metabolic inputs into changes in chromatin architecture and gene expression. EZH2 governs developmental cell fate through H3K27me3-mediated gene repression and is frequently dysregulated in cancer, where it promotes dedifferentiation, tumor progression, and metabolic reprogramming. Importantly, EZH2 activity is itself modulated by cellular metabolic status through posttranslational modifications, including phosphorylation, acetylation, methylation, ubiquitination, and O-GlcNAcylation, which influence its stability, catalytic activity, and chromatin-binding capacity. These modifications are responsive to nutrient availability and signaling pathways involving glucose, SAM, NAD, and other metabolic intermediates. Consequently, disruption of this finely tuned regulatory network can contribute to developmental abnormalities, metabolic dysfunction, and oncogenesis. In this review, we examine the molecular mechanisms governing EZH2 regulation and discuss how metabolic control of EZH2 shapes chromatin dynamics, cell fate decisions, and disease pathogenesis. Elucidating how metabolic signals modulate EZH2 activity will advance our understanding of development and disease while uncovering potential therapeutic opportunities to target metabolism-driven epigenetic dysregulation. - Source: PubMed
Publication date: 2026/07/23
Ansari Suraiya AnjumEmerald Bright Starling