Human EpCAM _CD326 Protein Vector: HEK293
- Known as:
- Human EpCAM _CD326 Protein Vector: HEK293
- Catalog number:
- 10115-H01H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human EpCAM _CD326 Protein Vector: HEK293
Related genes to: Human EpCAM _CD326 Protein Vector: HEK293
- Gene:
- EPCAM NIH gene
- Name:
- epithelial cell adhesion molecule
- Previous symbol:
- M4S1, MIC18, TACSTD1
- Synonyms:
- Ly74, TROP1, GA733-2, EGP34, EGP40, EGP-2, KSA, CD326, Ep-CAM, HEA125, KS1/4, MK-1, MH99, MOC31, 323/A3, 17-1A, TACST-1, CO-17A, ESA
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-02
- Date modifiied:
- 2019-04-23
Related products to: Human EpCAM _CD326 Protein Vector: HEK293
Related articles to: Human EpCAM _CD326 Protein Vector: HEK293
- Biomarkers based cancer cells discrimination plays an important role in the era of precision medicine. Single biomolecule-based cancer cells identification methods may lead to false positive results, while multiplexed and logic analysis methods have excellent accuracy and efficiency performances. In this work, a fluorescence composite coding strategy combining color and intensity was constructed with tandem shaped tetrahedral nano-string (TanTNS) as carrier and four Alexa Flour dyes as tags. More than 2 TanTNS codes were built by changing the types and numbers of AF dyes loaded on TanTNS. TanTNS probes prepared by the nanostructure of TanTNS codes binding with three bio-recognition unites successfully realized the specific fluorescence imaging of two miRNAs (miRNA 21 and miRNA-31) and two membrane proteins (EpCAM and PTK-7). Multiplexed fluorescence imaging of four molecules was demonstrated in single breast cell line by using TanTNS probes. Three beast cell types were logically distinguished based on fluorescence imaging of these four TanTNS probes in the co-cultured system. To further validate the specificity results and decode the genuine spatial information of targets, an independently developed fluorescence colocalization analysis method by using MATLAB was proposed. The TanTNS probes provided brand-new tools for precision medicine, expecting to be used for clinical liquid biopsy. - Source: PubMed
Publication date: 2026/04/21
Zhao XiaoshuangXu YiTian MeiGao YidanXu HuanhuaDai NingMi Xianqiang - Cold preservation is a critical logistical step in liver transplantation but induces ischemia-reperfusion injury (IRI), a key driver of early graft dysfunction. While bulk tissue assays capture global damage, they obscure the cell-type-specific transcriptional programs engaged during hypothermic storage. We utilized a multicellular human liver-on-chip model comprising Patient-Derived Organoids (PDOs), hepatic stellate cells (HSCs), liver sinusoidal endothelial cells (LSECs), and macrophages. Chips were exposed to 24-h static cold storage using either the clinical standard University of Wisconsin (UW) solution or a hyperbranched polyglycerol (HPG)-based formulation, followed by normothermic reperfusion. Single-cell RNA sequencing (scRNA-seq) was performed to map transcriptional trajectories across the preservation-reperfusion axis. We identified candidate solution-dependent transcriptional differences across cell types. PDOs from UW-preserved chips showed comparatively higher mean expression of inflammatory and oxidative stress-associated transcripts (IFI27, SAA1, HMOX1) and mitochondrially-encoded genes (MT-ND5) relative to HPG-preserved samples, which retained comparatively higher expression of homeostatic epithelial markers (EPCAM, KRT18). HSCs and LSECs in the UW group showed comparatively elevated expression of fibrosis-associated (COL1A1, TAGLN) and endothelial adhesion (ICAM1) transcripts. Ligand-receptor interaction modelling identified candidate inflammatory communication axes, including chemokine signaling interactions (CXCL1, CCL20) between macrophages and epithelial compartments, with higher predicted activity under UW preservation. This study provides an exploratory, high-resolution map of cell-type-specific transcriptional patterns associated with hypothermic preservation in a liver-on-chip model. Our findings suggest that preservation solution chemistry is associated with distinct transcriptional signatures spanning stress response, mitochondrial, and intercellular signaling pathways. Transcriptional patterns in HPG-preserved cells were consistent with comparatively attenuated injury responses; however, these observations are hypothesis-generating and require independent biological replication and functional validation, including metabolic flux assays and ROS production measurements before conclusions regarding mitochondrial protection or clinical preservation efficacy can be drawn. - Source: PubMed
Publication date: 2026/05/02
Mugaanyi JosephHuang JingYe ShengFang JiongzeMusinguzi ArthurDai LeiLu Caide - Cancer stemness drives malignant progression and drug resistance in hepatocellular carcinoma (HCC). Although mitochondrial dynamics are known to influence HCC development, the precise mechanisms linking mitochondrial function to stemness remain largely elusive. Integrating bulk and single-cell transcriptomics, we identified Butyrophilin Subfamily 3 Member A3 (BTN3A3) as a novel oncogene driving HCC stemness. BTN3A3 depletion markedly reduced sphere formation, stemness-related gene expression, and the percentage of CD90+/EpCAM+ cancer stem cells. Rescue experiments confirmed that BTN3A3 promotes HCC cell proliferation, migration, and invasion. Furthermore, BTN3A3 depletion sensitized HCC cells to sorafenib by inducing ROS accumulation and apoptosis. Mechanistically, mass spectrometry and Co-IP identified TOMM22 as a key mitochondrial interactor of BTN3A3. Crucially, sorafenib stress actively promotes BTN3A3 mitochondrial translocation, where it shields TOMM22 from ubiquitin-proteasome-dependent degradation. BTN3A3 deficiency led to TOMM22 depletion, mitochondrial fragmentation, and impaired oxidative phosphorylation (OXPHOS) and ATP production. Importantly, silencing TOMM22 reversed BTN3A3-mediated stemness and sorafenib resistance. In vivo orthotopic xenograft models and patient-derived organoids (PDOs) further validated that BTN3A3 correlates with stemness and malignant tumor growth. Utilizing 5E08, a pan-BTN3 monoclonal antibody, markedly suppressed tumor growth and concurrently downregulated TOMM22 expression in vivo. In conclusion, our study unveils a previously unrecognized non-immunological role for BTN3A3 in mitochondrial reprogramming. We demonstrate that BTN3A3 drives HCC stemness and drug resistance by preventing TOMM22 ubiquitination to maintain mitochondrial homeostasis. These findings position BTN3A3 as a promising therapeutic target, with the pan-BTN3 monoclonal antibody 5E08 offering a potential strategy to overcome stemness-driven malignancy and resistance in HCC patients. - Source: PubMed
Publication date: 2026/04/30
Kang XiaofengLei GuanglinHou XiaoboDu YimengXu MinghaoXue ChunyuanLiu DonghuiJia SonghaoShan JingboTang ChuanhaoXu XiaojieXu An - Circulating tumor cells (CTCs) serve as critical biomarkers for diagnosis, treatment monitoring, and prognosis evaluation of lung cancer. However, their trace abundance in blood makes the development of integrated technologies for CTCs isolation, enrichment, and detection with both high specificity and sensitivity a key bottleneck for clinical translation. This study proposed a novel cascade cell-assisted enhanced fluorescence strategy that integrates dual-targeting recognition, cell-mediated cascade assembly, and enzymatic amplification. This dual-targeting strategy achieves efficient capture and enrichment of human non-small cell lung cancer cell line A549 cells through EpCAM antibodies, and uses dual-aptamer probe-mediated EGFR recognition to further improve detection specificity. Subsequently, cascade assembly of acute lymphoblastic leukemia CCRF-CEM cells around target cells combined with enzyme-catalyzed signal amplification constructed a highly sensitive fluorescence-based detection system, with a linear range of 10-10 cells/mL, a limit of detection (LOD) as low as 10 cells/mL, and recovery rates of 94.25%-105.41%. Importantly, clinical validation using whole blood samples from lung adenocarcinoma patients ( = 30) and healthy donors ( = 23) showed significant differentiation ( < 0.05, AUC of 0.728), underscoring its diagnostic potential. Moreover, its modular expandability allows extension to other tumor CTCs detection by replacing target recognition units. - Source: PubMed
Publication date: 2026/04/30
Wang YifuBulale ShajidanWang YaSong LuluLi RuoweiHe LeiliangZhang Shaokai - Postoperative recurrence and infection continue to pose major challenges after tumor resection. To address these, we developed a multifunctional nanocomposite hydrogel, designated as Gel@CAR-M@Mn@ELE. It is constructed by encapsulating CAR-M@Mn@ELE and immunomodulatory/antibacterial Dendrobium officinale polysaccharide (DOP) within a quaternary ammonium-modified gelatin methacryloyl hydrogel matrix. The CAR-M@Mn@ELE not only loads elemene (ELE) into porous Mn nanozymes (Mn NPs) but is also coated with EpCAM-targeting chimeric antigen receptor-engineered 293T cell membranes (CAR-M). Notably, through multiple modifications, the catalytic activity of Mn NPs has been preserved. In vitro studies demonstrated that CAR-M@Mn@ELE selectively targeted and killed 4T1 cancer cells (EpCAM), while the hydrogel exhibited potent antibacterial activity against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). In vivo evaluation using a post-tumor-resection mouse model confirmed that Gel@CAR-M@Mn@ELE significantly suppressed tumor recurrence and prolonged survival. The combination of bioactive components within the hydrogel modulated the immunosuppressive tumor microenvironment, thereby enhancing its immunotherapeutic efficacy. Additionally, in a bacterial wound infection model, the hydrogel effectively inhibited bacterial growth and accelerated wound healing. The Gel@CAR-M@Mn@ELE offers a novel and promising strategy, supported by experimental evidence, for concurrently addressing the critical post-surgical challenges of tumor recurrence and wound infection. - Source: PubMed
Publication date: 2026/04/29
Qin YatingYao KeLin YanLi XinyueLiu YifanLi YilinLi YapingWang Shuling