Recombinant human EpCAM /CD326 Protein
- Known as:
- Recombinant H. sapiens EpCAM /CD326 Protein
- Catalog number:
- epcam-011
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant human EpCAM /CD326 Protein
Related genes to: Recombinant human EpCAM /CD326 Protein
- 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: Recombinant human EpCAM /CD326 Protein
Related articles to: Recombinant human EpCAM /CD326 Protein
- Primary Sjögren's syndrome (pSS) is characterized by salivary gland-centered immune dysregulation, in which an imbalanced T follicular helper (Tfh)/T follicular regulatory (Tfr) axis drives aberrant follicular responses and glandular dysfunction. In this study, we developed an engineered exosome-based therapeutic platform (Exo@But-αEpCAM) by combining CD4 T cell-derived exosomes, anti-EpCAM antibody-mediated targeting, and sodium butyrate as a Foxp3 agonist. The engineered exosomes exhibited stable antibody modification and efficient drug loading while preserving vesicle integrity and biosafety. Under inflammation-mimicking conditions relevant to pSS, Exo@But-αEpCAM displayed microenvironment-sensitive drug release. In vitro studies using peripheral blood mononuclear cells (PBMCs) from patients with pSS demonstrated that Exo@But-αEpCAM effectively restored the Tfh/Tfr balance by enhancing Foxp3-associated regulatory pathways and suppressing Tfh-related signaling, leading to reduced B cell activation. In a murine model of pSS, targeted exosome treatment preferentially accumulated in salivary glands, significantly improved salivary secretion, alleviated histopathological inflammation, and re-established local immune homeostasis without inducing systemic toxicity. Mechanistically, transcriptomic and proteomic analyses revealed that Exo@But-αEpCAM attenuated Tfh-driven follicular responses through inhibition of the IL-21R/STAT3 signaling axis. Collectively, this work presents a targeted and immunoregulatory exosome-based strategy that reconstructs immune homeostasis rather than broadly suppressing immunity, providing a promising therapeutic approach for pSS. - Source: PubMed
Publication date: 2026/04/21
Tian BailingLi QiyuChang BohanZhao Shan - Lu-PSMA-617 represents a transformative treatment for metastatic castration-resistant prostate cancer (mCRPC), yet biomarkers of benefit beyond prostate-specific membrane antigen positron emission tomography (PSMA-PET) imaging remain lacking. Here, we present findings from a prospective study of 100 mCRPC patients receiving Lu-PSMA-617, using shotgun proteomics to profile plasma-derived extracellular vesicle (EV) proteins alongside PSMA-positive circulating tumor cell (CTC) enumeration. We identify 5,137 EV-derived proteins, including the cell-surface targets PSMA, B7-H3, Trop-2, and STEAP1, with high levels of these proteins associating with worse overall survival (OS). All four EV proteins positively correlate with molecular tumor volume on PSMA-PET imaging, serum PSA, and serum alkaline phosphatase. CTC subpopulations, including PSMA+/EpCAM+ and PSMA-/EpCAM+ cells, associate with worse progression-free survival (PFS) and OS. Pathway analysis reveals that p53 upregulation associates with poor PFS and OS, while an activated E2F pathway unexpectedly portends better PFS and OS. These findings support the integration of liquid biopsy proteomics into biomarker-driven mCRPC trials to improve patient stratification. - Source: PubMed
Publication date: 2026/04/20
Arafa Ali TBoytim EllaLudwig Megan LKollitz LilyYang TianzhongStorey Kathleen MBloom StuartJha GautamOkazaki IanRyan Charles JZorko Nicholas ASteinberger DanielCayci ZuzanZhao YingchunVillalta Peter WDehm Scott MHwang Justin HDrake Justin MAntonarakis Emmanuel S - Early detection of tumor-derived extracellular vesicles (EVs) enables noninvasive cancer diagnostics, but current assays often require wash steps and suffer from limited sensitivity. Here, we developed PlasDroplex, a wash-free digital plasmonic assay that detects tumor-derived extracellular vesicles via droplet-confined binding between EVs and antibody-functionalized gold nanoparticles (Ab-AuNPs), eliminating washing and multistep labeling processes. Plasma (10 μL) is coencapsulated with Ab-AuNPs targeting CD9, EpCAM, PSA, PSMA, and PD-L1 in picoliter droplets. Target binding induces AuNP clustering into plasmonic networks that generate bright "On" droplets, while "Off" droplets remain dark, enabling a wash-free optical readout within 1 h. Limits of detection were 2500-6700 EVs/mL with high reproducibility (CV < 3%). In 63 clinical samples, PSA- and PSMA-positive EVs yielded AUCs of 0.926 and 0.932 for prostate cancer, respectively, while PD-L1 EVs achieved an AUC of 0.998 for lung cancer. PlasDroplex enables rapid, marker-specific, digital droplet-based EV profiling from minimal plasma volumes. - Source: PubMed
Publication date: 2026/04/21
Jung Na KyungKarmacharya MamataChoi HyunminHa Hong KooOh In-JaeKim Mi-HyunRyu Jeong-SeonLim Chwee TeckKumar SumitCho Yoon-Kyoung - Lynch syndrome (LS) is one of the most widely recognized cancer susceptibility syndromes and is caused by germline mutations of the mismatch repair (MMR) genes , , , and . One of the less commonly known mechanisms is the deletion of the 3' end of the Epithelial Cell Adhesion Molecule () gene, which is closely situated to the gene promoter. Such deletion causes hypermethylation of the gene promoter and leads to its inactivation. This case reports a young adult diagnosed with two metachronous primary tumors due to a germline exon 9 deletion and subsequent gene inactivation, shedding light on one of the most underrecognised pathways of microsatellite instability. - Source: PubMed
Publication date: 2026/03/19
Kalfoutzou AretiRapti CleopatraAlmpanis ZannisBagiokou EleftheriaKalakos NikolaosLagopoulou VasilikiKolintzikis VasileiosOikonomakis AristeidisChaleplidis NikolaosRamfidis Vasileios - Oncolytic viruses (OVs) are designed to selectively infect, proliferate within, and destroy cancer cells while concurrently eliciting robust antitumor immune responses. Notwithstanding their significant potential, inadequate tumor selectivity and restricted treatment efficacy persist as substantial barriers to wider clinical utilization. This review rigorously evaluates current advancements in OV engineering designed to address these issues. Transcriptional targeting, which employs tumor-specific promoters like hTERT, E2F1, and hypoxia-inducible elements, microRNA detargeting, and the redirection of viral entry towards tumor-associated antigens such as EGFR, HER2, and EpCAM, alongside multi-layered logic-gated regulatory systems, represent strategies to augment tumor specificity. To bolster anticancer efficacy, OVs have been modified with immunomodulatory agents, including cytokines (GM-CSF, IL-12), immune checkpoint inhibitors (anti-PD-1, anti-CTLA-4), chemokines, and stroma-degrading enzymes (hyaluronidase, relaxin). Subsequent advancements encompass nanoparticle encapsulation, carrier-cell transport mechanisms, metabolic reprogramming strategies, and synergistic combinations with immunotherapy, chemotherapy, or radiotherapy. Furthermore, systems and synthetic biology techniques are enabling the development of advanced "smart" OVs, which possess the capacity for real-time detection and adaptation within the tumor microenvironment. These combined methodologies present considerable promise for enhancing the safety profile, intratumoral distribution, and overall therapeutic efficacy of oncolytic virotherapy. - Source: PubMed
Publication date: 2026/04/16
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