Ask about this productRelated genes to: EpCAM antibody (FITC)
- 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: EpCAM antibody (FITC)
Related articles to: EpCAM antibody (FITC)
- Antibody-drug conjugates (ADCs) are transforming the therapeutic landscape of solid tumours. Both patient selection and ADC efficacy in triple-negative breast cancer (TNBC) and epithelial ovarian cancer (EOC) are impacted by target antigen expression, which is often heterogeneous. Single tissue biopsies cannot capture this spatial heterogeneity, creating a need for real-time assessment to guide treatment. Circulating tumour cells (CTCs) may serve as minimally invasive biomarkers that can reflect ADC target expression. The aim of this study was to assess the detectability of clinically relevant ADC targets on CTCs in TNBC and EOC. - Source: PubMed
Publication date: 2026/06/30
Henderson Brian DMcMahon LaurenLewis FayeMarion CarolineHurley SineadGately KathyNarinda IreneKanjuga MarikaNorris LucyMartin CaraConlon NeilO'Driscoll LorraineSaadeh Feras AbuO'Gorman CatherineMaguire Patrick JKamran WaseemIbrahim ElzahraCadoo Karen AColeman NiamhO'Leary John JWard Mark PO'Toole Sharon A - Infections by can rapidly progress from mucosal colonization to invasive disease, but how these bacteria efficiently breach epithelial barriers is unclear. Here, we define a coordinated two-component virulence strategy in biotype sobria ( sobria) involving a secreted serine protease (ASP) and aerolysin. In polarized T84 monolayers, wild-type infection caused rapid transepithelial electrical resistance (TEER) loss and degradation of junctional/adhesion proteins. An ASP-deficient strain exhibited delayed barrier collapse with reduced cleavage of ZO-1/2/3 and EpCAM, and purified ASP restored these effects, indicating ASP is required but alone insufficient for full disruption. A transposon screen identified aerolysin and secretion-related genes as key contributors to junctional damage. Mechanistically, ASP directly converted recombinant pro-aerolysin into a hemolytically active toxin , linking protease activity to toxin maturation. Functionally, ASP and aerolysin synergized to promote bacterial translocation across epithelial monolayers with marked sequence dependence; pro-aerolysin pretreatment enhanced ASP-mediated degradation of ZO proteins, claudin-7, and EpCAM. ASP further cleaved EpCAM at multiple extracellular sites, compromising adhesion and junctional homeostasis. Together, these findings establish an ASP-aerolysin pathway that couples toxin activation with junctional proteolysis to drive structural epithelial breaches.IMPORTANCE infections can rapidly progress from intestinal colonization to invasive disease, yet the molecular steps enabling epithelial breach are unclear. We show that sobria uses a coordinated two-factor pathway in which serine protease (ASP) both activates the pore-forming toxin aerolysin and directly cleaves key junctional/adhesion proteins, including ZO-1/2/3 and EpCAM. Aerolysin primes cells for enhanced ASP-mediated proteolysis in an order-dependent manner, converting TEER loss into a physical barrier rupture that permits massive bacterial translocation. Targeting ASP-aerolysin cooperation may provide a rational anti-virulence strategy. - Source: PubMed
Publication date: 2026/07/10
Kobayashi HidetomoSeike SoshiTakahashi EizoOkamoto KeinosukeYamanaka Hiroyasu - Despite advances in IgG-based cancer immunotherapy, challenges remain in effectively engaging innate immune responses against solid tumors. Here, IgA antibodies hold promise due to their ability to activate neutrophils and macrophages. We present a novel retargeted adenovirus-mediated approach that transforms cancer cells into "biofactories" for localized production of monomeric or dimeric IgA antibodies and a CD47 blocker to potentiate the effect of IgA antibodies. With our approach, tumor cells effectively produced IgA antibodies against tumor antigens such as EGFR or EpCAM and a soluble SIRPα-Fc fusion protein, which blocks the CD47-SIRPα axis. In a perfused tumor-on-a-chip model, locally produced IgA triggered neutrophil- and macrophage-mediated tumor cell killing, further potentiated by SIRPα-Fc co-production. In FcαRI-transgenic, tumor-bearing mice, intratumoral adenoviral injection induced strong local IgA and SIRPα-Fc expression, immune cell infiltration, and more than 50% tumor volume reduction after a single treatment. We found that dimeric IgA exerts stronger effects than monomeric IgA. Together, these results demonstrate that adenovirus-mediated, tumor-restricted delivery of IgA antibodies and CD47 blockade effectively engages innate immune mechanisms and has therapeutic promise. - Source: PubMed
Publication date: 2026/07/07
Chernyavska MariyaHartmann K PatriciaJansen J H MarcoBaumann NiklasKolibius JonasBrücher DominikKristoforus TheodoraPeters Rens H WHuijs LucasLaarveld DaphneWeiss FabianBurger RenateLustig MartaGimenez de Assis NadineSchmid MarkusLeusen Jeanette H WValerius ThomasPlückthun AndreasVerdurmen Wouter P R - Asthma is a heterogeneous airway disease characterized by chronic inflammation, airway hyperresponsiveness (AHR), and airway remodeling. Previously, we identified Protocadherin-1 (PCDH1) as a susceptibility gene for AHR, a hallmark of asthma. PCDH1 is an adhesion molecule, highly expressed in the airway epithelium. However, its role in AHR, airway inflammation, and remodeling is not fully understood. We generated Pcdh1-deficient mice to test whether Pcdh1 loss increases susceptibility to developing asthma features, including AHR, airway inflammation, and remodeling at baseline or upon challenge with house-dust mite (HDM) or Respiratory Syncytial Virus (RSV). Pcdh1-deficient mice were viable and expressed a truncated form of Pcdh1. Naive Pcdh1-knockout (KO) mice displayed lower lung compliance than wild-type (WT) littermate controls. The barrier integrity of cultured tracheal epithelial cells isolated from KO and HET was lower than that of WT mice. Intriguingly, single-cell RNA sequencing analysis of tracheal epithelial cells revealed higher proportions of basal cells and a unique Hillock-like cell population in KO mice, while ciliated cells were lower in proportion. Upon HDM exposure, but not RSV infection, Pcdh1-KO mice showed increased AHR and lower lung compliance compared to WT mice. Altogether, we demonstrate that Pcdh1 deficiency in mice results in loss of airway epithelial barrier integrity and reduced lung compliance at baseline and after HDM exposure, indicating a potential role in airway remodeling. These changes are accompanied by alterations in airway epithelial differentiation. In conclusion, this novel mouse model points towards a role of Protocadherin-1 in remodeling of the airways, epithelial differentiation and barrier integrity. - Source: PubMed
Publication date: 2026/07/07
Ly Bao-HanBrouwer UilkeHesse LauraKumawat Kuldeepvan Gosliga DjokePetersen Arjen HNijboer Susanden Boef Lisette EJonker Marnix RKarsenberg RenskeDalenberg Jelle RTimens WimBurgess Janette KTeichmann Sarah Avan Oosterhout Antoon J MLambrecht Bart NMeyer Kerstin Bvan Roy FransHochepied TinoBont Louisvan Hengel JolandaNawijn Martijn CKoppelman Gerard H - Programmed death-ligand 1 (PD-L1) blockade improves outcomes in patients with various malignancies; however, biomarkers for monitoring treatment responses are lacking. This study presents a surface-enhanced Raman scattering (SERS)-based platform for the ultrasensitive detection of PD-L1 on circulating epithelial cell adhesion molecule-positive (EpCAM) extracellular vesicles (EVs). The platform is validated using interferon-gamma-treated epithelial tumor cell line-derived EVs. The platform is further applied to paired pre- and post-treatment plasma samples from patients with non-small-cell lung cancer (n = 140) and head and neck squamous cell carcinoma (n = 73) receiving anti-PD-(L)1 immunotherapy. Dynamic changes in PD-L1 expression on EV are shown to correlate with clinical outcomes. A post-treatment decrease in PD-L1 expression on EpCAM EVs (EpCAM EV PD-L1) is associated with improved 5-year progression-free and overall survival. These results establish EpCAM EV PD-L1 as a dynamic, non-invasive biomarker for monitoring immunotherapy responses and demonstrate the utility of SERS-based profiling in predicting long-term responses to immune checkpoint blockade. - Source: PubMed
Publication date: 2026/07/03
Mun ByeonggeolKim JinyoungKim Chang GonGo SeokhyeongHan MinaOuck YujinJang SoojinSon Seong UkKim GaminSon WonrakKim EunjungHong Min HeeYeo Ja HyunLim Eun-KyungKim Hye RyunHaam Seungjoo