EpCAM Assay Portfolio Service

Background Functions What We Can Offer Publication Why Choose Us FAQs Customer Review Related Services Contact Us

Epithelial Cell Adhesion Molecule (EpCAM) Structure

Epithelial cell adhesion molecule (EpCAM, also known as CD326 or TACSTD1) is a type I transmembrane glycoprotein, consisting of 314 amino acids with 40 kDa in molecular weight. EpCAM is comprised of an extracellular domain with epidermal growth factor (EGF) and thyroglobulin repeat-like domains, a single transmembrane domain, and a short 26-amino acid intracellular domain called EpICD. Two EpCAM subunits form a heart-shaped dimer on the cell surface. EpCAM is expressed in a variety of human epithelial tissues, cancers, progenitor, and stem cells, and is also a cell surface marker on various stem and progenitor cells. EpCAM is highly expressed in epithelial cancer, including colon and breast cancer.

Fig.1 Diagrammatic depiction of EpCAM structure. (OA Literature)Fig.1 Structural overview of EpCAM.1, 3

Functions of EpCAM

Cell Adhesion.

EpCAM is a homophilic Ca2+-independent cell-cell adhesion molecule in cells. While it can modulate E-cadherin-mediated adhesion, it is also highly expressed in tumor tissues, which often lose organized adhesive structures and cell polarity.

Cell Junction.

EpCAM is essential for cell junctions. It interacts with several important cell adhesion molecules (CAMs) and regulates adhesive structures between cells and the cell-matrix, including adherens junctions, tight junctions, desmosomes, and hemidesmosomes.

Cell Proliferation.

Several in vitro and in vivo studies have shown that overexpression of EpCAM induces cell proliferation, whereas downregulation of EpCAM decreases cell proliferation.

EpCAM and Stem Cell.

EpCAM plays an important role in the induction and/or maintenance of proliferation and cellular differentiation of progenitors, stem cells, induced pluripotent stem cells, cancer cells, and cancer stem cells.

Epithelial to Mesenchymal Transition (EMT).

The regulation of EpCAM during EMT is context-dependent. Some studies show downregulation, while others suggest a promoting role. Interestingly, EpCAM can also suppress ERK and SNAIL2, creating a double-negative feedback loop.

Migration and Invasion.

EpCAM's role in cancer cells is conflicting and context-dependent. It may promote breast cancer invasion, while its knockdown can increase migratory capacity in esophageal carcinoma, a process linked to increased vimentin expression.

What We Can Offer?

EpCAM is a pan-epithelium marker, which is expressed in a great variety of differentiated epithelia. Importantly, EpCAM is the central target molecule for the enrichment and characterization of systemic tumor cells with prognostic and metastatic potential. Creative Biolabs provides a full set of EpCAM assay portfolio services for research, including but not limited to:

Publication

This review explores the critical role of EpCAM in oral cancer stem cells (CSCs), emphasizing its impact on metastasis, tumorigenicity, and therapeutic resistance. EpCAM, a transmembrane glycoprotein, regulates key pathways like Wnt/β-catenin and EGFR, driving CSC self-renewal, EMT, and immune evasion. The authors highlight EpCAM's involvement in metabolic reprogramming, epigenetic regulation, and crosstalk with the tumor microenvironment, underscoring its potential as a diagnostic biomarker and therapeutic target. Advances in EpCAM-targeted therapies—including monoclonal antibodies, CAR-T/NK cells, and aptamer-based systems—are discussed, alongside challenges like resistance mechanisms and heterogeneous expression. The review calls for further research to optimize therapeutic strategies and improve clinical outcomes, offering valuable insights for researchers and clinicians in oncology.

Fig.2 EpCAM-dependent signaling networks in malignancy. (OA Literature)Fig.2 The impact of EpCAM signaling on tumor development and metastasis.2, 3

Why Choose Us?

EpCAM, a transmembrane glycoprotein overexpressed in many cancers, plays a critical role in tumor progression, metastasis, and cancer stem cell maintenance. Its complex signaling pathways and involvement in metabolic reprogramming make it both a promising therapeutic target and a significant research challenge.

At Creative Biolabs, we combine deep scientific expertise with cutting-edge technology to help you navigate this complexity. Our specialized assays and robust platforms deliver reliable, reproducible data, empowering your EpCAM-targeted drug discovery efforts. Whether you're exploring monoclonal antibodies, CAR-T therapies, or novel inhibitors, our tailored solutions provide the precision and insight needed to accelerate breakthroughs.

Partner with us to overcome the challenges of EpCAM research and drive innovation in oncology.

FAQs

Q1: How does your service address potential off-target toxicity to normal epithelial cells?

A1: We assess your candidate's specificity and therapeutic window using binding assays and functional cell-based tests across EpCAM-positive tumor and normal cell lines for a clear safety profile.

Q2: Can you help us characterize the EpCAM expression on our specific cancer cell lines or patient samples?

A2: Absolutely. Our biomarker analysis services use advanced techniques like flow cytometry and immunofluorescence to quantify EpCAM expression levels. This is a crucial step for target validation and patient stratification, ensuring your therapy targets the right population.

Q3: How do your assays account for the dynamic nature of EpCAM expression, such as in circulating tumor cells (CTCs) undergoing EMT?

A3: Our multi-faceted approach includes assays that analyze both EpCAM-positive and EpCAM-negative populations, along with other markers. This provides a complete understanding of how your molecule performs against heterogeneous and evolving tumor cell populations.

Customer Review

  • Robust Data
    Creative Biolabs' comprehensive report provided a level of detail and data quality that was essential for our regulatory submissions. The insights into EpCAM's binding kinetics and cellular efficacy were invaluable. - Dr. L***n
  • Expert Collaboration
    The collaborative approach of the Creative Biolabs team was fantastic. Their expertise in EpCAM biology helped us troubleshoot an unexpected resistance mechanism and pivot our strategy effectively. - A***w

Related Services

To further support your research, Creative Biolabs offers several complementary services that are often used in conjunction with our EpCAM assay portfolio:

TCR-T and CAR-T/NK Cytotoxicity Assay

Creative Biolabs provides T/NK cell cytotoxicity assays to assess drug candidates and immunotherapy strategies. Using advanced instruments, they can perform long-term assays on various cancer and healthy cell lines, including iPSCs, to evaluate cytotoxicity and safety.

Learn More →

Single Cell Immune Profiling

Creative Biolabs offers flow cytometry analysis and intracellular staining to understand the impact of immune cell therapy. Their streamlined workflow allows for the identification and analysis of multiple immune cells, revealing the diversity of specific recombinant CAR-immune cells.

Learn More →

Contact Us

Creative Biolabs provides a complete portfolio of tumor marker assays, such as the EpCAM assay portfolio service. We are continually expanding our portfolio by adding new tumor marker assays and applications and broadening our network with competent partners. Our goal is to help our clients achieve research goals as quickly and as easily as possible. Please feel free to contact us.

References

  1. Liu, Yiyang, et al. "Understanding the versatile roles and applications of EpCAM in cancers: from bench to bedside." Experimental hematology & oncology 11.1 (2022): 97. DOI: https://doi.org/10.1186/s40164-022-00352-4
  2. Chang, Chuan-Hsin, et al. "EpCAM signaling in oral cancer stem cells: implications for metastasis, tumorigenicity, and therapeutic strategies." Current Issues in Molecular Biology 47.2 (2025): 123. DOI: https://doi.org/10.3390/cimb47020123
  3. Distributed under Open Access license CC BY 4.0, without modification.
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