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EC109 Xenograft Model Service for Esophageal Squamous Cell Carcinoma (ESCC)

EC109 xenograft model for Esophageal Squamous Cell Carcinoma (ESCC) preclinical research.

The EC109 xenograft model provides a robust preclinical platform for evaluating therapeutic efficacy against esophageal squamous cell carcinoma (ESCC), enabling researchers to assess tumor growth dynamics, drug response profiles, and molecular biomarker changes in an immunodeficient host environment. Alfa Cytology delivers validated EC109 xenograft models with stringent quality control, offering customizable study designs that include subcutaneous and orthotopic implantation, multi-arm dosing regimens, and comprehensive endpoint analyses to accelerate your preclinical oncology pipeline.

Overview of EC109 Xenograft Model for Esophageal Squamous Cell Carcinoma (ESCC)

EC109 is a human esophageal squamous cell carcinoma (ESCC) cell line originally established in 1973 from a middle-esophageal tumor specimen of a female patient. As an epithelial-like, adherent cell line, EC109 exhibits a doubling time of approximately 28.6 hours under standard culture conditions and expresses canonical epithelial markers including cytokeratins and EpCAM (CD326). The cell line harbors molecular alterations characteristic of ESCC, with enrichment in pathways governing cell cycle regulation, TP53 signaling, Hippo pathway modulation, and Wnt signaling transduction. EC109 cells demonstrate robust tumorigenicity in immunodeficient murine hosts, forming well-defined xenograft tumors that recapitulate key histopathological features of human ESCC, including keratin pearl formation and stratified squamous differentiation. These characteristics render EC109 a widely utilized model for investigating cancer cell proliferation, migration, invasion, autophagy modulation, and drug sensitivity in the context of esophageal malignancy.

In xenograft applications, EC109 tumors maintain consistent growth kinetics and exhibit measurable responses to standard-of-care agents such as cisplatin, 5-fluorouracil, and paclitaxel, while also serving as a parental platform for generating drug-resistant sublines (e.g., EC109/CDDP) through pulse-selection protocols. The model supports both subcutaneous and orthotopic implantation strategies, with the latter enabling studies of local tumor invasion and lymph node metastasis that more closely mimic clinical disease progression. Researchers frequently leverage EC109 xenografts to evaluate novel therapeutic modalities, including targeted antibodies, small-molecule inhibitors, and combination regimens, as well as to investigate biomarker-driven patient stratification strategies in preclinical settings.

Reference figures for EC109 cell-related literature.Figure 1. Flow cytometric analysis of side population (SP) in EC109 cells and RR-EC109 cells. (Shen, Yanru, et al., 2022)

Cell Line Information: EC109

The EC109 cell line (also cataloged as Eca-109, EC-109, or Eca109) is a continuously propagated human ESCC line with the following documented characteristics:

Attribute Description
Cell Line Name EC109 (Eca-109; EC-109; Eca109)
Disease Esophageal Squamous Cell Carcinoma (ESCC)
Tissue of Origin Esophagus (middle esophageal region)
Cell Type Epithelial
Morphology Epithelial-like, polygonal, adherent monolayer
Species Human (Homo sapiens)
Gender Female
Ethnicity Chinese
Year Established 1973
Doubling Time ~28.6 hours (28.57 +/- 0.12 hours)
Growth Conditions 37 degrees C, 5% CO2; RPMI 1640 + 10% FBS
Biosafety Level BSL-1
Tumorigenicity Tumorigenic in BALB/c nude mice and immunodeficient strains
Key Markers Cytokeratins, EpCAM (CD326), c-Met expression documented
Molecular Pathways Cell cycle regulation, TP53, Hippo, Wnt signaling enrichment
Drug Sensitivity Responsive to cisplatin, 5-FU, paclitaxel; resistant subline EC109/CDDP available
Applications Proliferation, migration, invasion, apoptosis, autophagy, radiosensitivity, and drug resistance studies
Synonyms / Catalog IDs CVCL_6898; CCRID: 3111C0001CCC000246; ChEMBL-Cells: CHEMBL3308477

Our Services

Alfa Cytology offers fully validated EC109 xenograft models developed under rigorous quality assurance protocols, ensuring consistent tumor take rates, predictable growth kinetics, and reproducible pharmacological responses. Our preclinical team provides end-to-end study management---from model establishment and in-life monitoring to terminal endpoint analysis---allowing you to generate high-confidence data for IND-enabling studies and peer-reviewed publications. Whether your program requires standard subcutaneous implantation or advanced orthotopic surgical models, Alfa Cytology tailors every study parameter to align with your therapeutic hypothesis and regulatory milestones.

Workflow of EC109 Xenograft Model Construction

The construction of EC109 xenograft models follows a standardized, multi-phase workflow designed to ensure tumor viability, reproducible growth parameters, and data integrity across study cohorts. Each phase incorporates quality checkpoints to confirm cell line authentication, sterility, and tumorigenic potential prior to client-specific study initiation.

  1. Cell Line Authentication & Expansion: EC109 cells are revived from authenticated master stocks and verified by short tandem repeat (STR) profiling against reference databases. Cells are expanded under standardized culture conditions (RPMI 1640 supplemented with 10% FBS, 37 degrees C, 5% CO2) to generate sufficient inoculum for implantation, with viability confirmed by trypan blue exclusion (>95% viability required).
  2. Mouse Strain Selection & Preparation: Immunodeficient host strains---most commonly BALB/c nude mice or NOD-SCID mice---are selected based on study objectives. Animals are acclimatized for a minimum of five days, with health status verified by veterinary inspection prior to tumor cell inoculation.
  3. Tumor Cell Inoculation: EC109 cells are harvested during logarithmic growth phase, washed in sterile PBS, and resuspended in a 1:1 mixture of PBS and Matrigel or serum-free medium. For subcutaneous models, 1x10^6 to 5x10^6 cells are injected into the flank region; for orthotopic models, cells are surgically implanted into the esophageal wall or injected via periesophageal injection under anesthesia.
  4. Tumor Establishment Monitoring: Implanted animals are monitored daily for health status, with tumor palpation initiated 3-5 days post-inoculation. Tumor dimensions are measured twice weekly using digital calipers, and volumes are calculated via the modified ellipsoid formula (V = 0.5 x length x width^2). Tumors are permitted to reach a target volume of 100-200 mm^3 prior to randomization and treatment initiation.
  5. Study Randomization & Treatment: Animals bearing established tumors are randomized into treatment and vehicle-control cohorts based on tumor volume and body weight to minimize inter-group variability. Dosing regimens are administered according to client protocols, with schedules ranging from daily to weekly intervals, and dosing routes including intraperitoneal, intravenous, or oral gavage.
  6. Endpoint Analysis & Sample Collection: At study termination, tumors are excised, weighed, and processed for downstream analyses. Standard endpoints include tumor growth inhibition (TGI), tumor regression rate, and body weight change. Tissue samples are preserved in formalin for histopathology (H&E, IHC), snap-frozen for protein/RNA extraction, or dissociated for flow cytometry and cell analyses.

Workflow for the establishment of EC109 cell line-derived xenograft (CDX) models.Figure 2: Schematic workflow illustrating the derivation and construction of the EC109 Xenograft Model at Alfa Cytology.

Case Study-EC109 Xenograft Model Development

In a representative preclinical engagement, Alfa Cytology established subcutaneous EC109 xenografts in immunodeficient mice to evaluate a novel therapeutic candidate targeting the EGFR/ERK1/2 signaling axis. Tumors reached the target enrollment volume within 14-18 days post-implantation, exhibiting consistent growth kinetics across all animals. Following randomization, the treatment cohort received the investigational compound via intraperitoneal administration on a biweekly schedule, while the control cohort received vehicle only. Preliminary data indicated dose-dependent tumor growth inhibition, with the high-dose group demonstrating a measurable reduction in tumor volume relative to vehicle controls by the second week of treatment. Terminal analyses included H&E staining for morphological assessment and immunohistochemical evaluation of proliferation markers (Ki-67) and apoptosis indicators (cleaved caspase-3), providing a comprehensive dataset for client decision-making. Specific numerical values and statistical outcomes are available upon formal study inquiry and can be customized to meet publication or regulatory submission requirements.

Case Study-EC109 Xenograft Model Development.

Why Choose Alfa Cytology?

Alfa Cytology combines scientific rigor with operational flexibility to deliver EC109 xenograft models that meet the highest standards of preclinical oncology research. Our integrated service platform ensures seamless transition from model development to full-scale efficacy studies, supported by experienced study directors and dedicated project managers.

  • Validated cell line authentication via STR profiling and mycoplasma screening for every batch.
  • Customizable study designs encompassing subcutaneous, orthotopic, and metastatic model configurations.
  • Real-time tumor monitoring with electronic data capture and secure client portal access.
  • Comprehensive endpoint analysis including histopathology, biomarker immunohistochemistry, and molecular profiling.
  • Dedicated project management with weekly progress updates and rapid response to protocol amendments.
  • Competitive timelines with tumor establishment typically achieved within 2-3 weeks post-implantation.

Contact Us

Ready to advance your ESCC therapeutic program with a validated EC109 xenograft model? Please reach out to us today via our inquiry form or email to learn more about our EC109 Xenograft Model services.

Reference

  1. Shen, Yanru, Lihui Yang, and Lei Li. "Cancer stem-like cells contribute to paclitaxel resistance in esophageal squamous cell carcinoma." International journal of clinical and experimental pathology 15.4 (2022): 183.

For research use only. Not intended for any clinical use.

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