ECC-1 Xenograft Model Service for Endometrial Cancer

The ECC-1 xenograft model is a well-established, hormone-responsive preclinical platform for evaluating therapeutic efficacy against endometrial adenocarcinoma, leveraging a cell line with high estrogen receptor expression and luminal epithelium characteristics to closely mimic type I endometrial cancer biology. At Alfa Cytology, we specialize in delivering validated, high-quality ECC-1 xenograft models tailored to your preclinical research needs. Our experienced team ensures reproducible tumor growth, comprehensive endpoint analysis, and flexible study designs to accelerate your drug development pipeline from early-stage screening to late-phase efficacy evaluation.
Overview of ECC-1 Xenograft Model for Endometrial Cancer
The ECC-1 cell line was originally established by P.G. Satyaswaroop from a well-differentiated endometrial adenocarcinoma derived from a 39-year-old female patient. It is classified as a Type I (endometrioid) endometrial cancer cell line, exhibiting luminal epithelium characteristics and maintaining robust hormone responsiveness through estrogen receptor (ER-alpha and ER-beta), progesterone receptor (PR), and androgen receptor expression. ECC-1 cells also express p160 steroid receptor coactivators (NCOA1-3), the hyaluronate receptor CD44, SPP1, and CD55, all of which are implicated in endometrial implantation processes and tumor microenvironment interactions. The cell line carries key molecular alterations including PTEN missense mutation, TP53 missense mutations, and PI3K/Akt pathway activation, with high microsatellite instability, making it a representative model for studying hormone-driven endometrial carcinogenesis and targeted therapy responses.
In xenograft applications, ECC-1 cells demonstrate reliable subcutaneous tumor formation in immunodeficient mouse strains when supplemented with estrogen, typically reaching measurable tumor volumes within 2-4 weeks post-inoculation. The model has been extensively utilized to investigate PI3K/mTOR inhibitor sensitivity, antiestrogenic compound efficacy, Wnt pathway modulation, and platelet-derived growth factor (PDGF)-D mediated tumor invasion. Histologically, ECC-1 xenografts retain glandular differentiation patterns consistent with well-differentiated endometrial adenocarcinoma, providing a physiologically relevant platform for preclinical pharmacology and biomarker discovery in endometrial cancer research.
Figure 1. Validation of dysregulated proteins in shC1GALT1 ECC-1 cells. (Montero-Calle, Ana, et al., 2023)
Cell Line Information: ECC-1
ECC-1 is a well-characterized human endometrial adenocarcinoma cell line with extensive molecular, phenotypic, and genomic annotations. Below is a comprehensive summary of its key attributes:
| Attribute |
Details |
| Cell Line Name |
ECC-1 (also known as ECC1, EnCa1) |
| Cellosaurus ID |
CVCL_7260 |
| Disease |
Endometrial adenocarcinoma (Type I / Endometrioid) |
| Tissue of Origin |
Endometrium (primary tumor, in situ) |
| Patient Demographics |
Female, 39 years old at diagnosis |
| Ethnicity |
Japanese |
| Established By |
P.G. Satyaswaroop |
| Morphology |
Luminal epithelium characteristics; well-differentiated glandular architecture |
| Population Doubling Time |
~19-41 hours (within range of Type I EC cell lines) |
| Hormone Receptor Status |
High ER-alpha and ER-beta expression; PR and androgen receptor positive; hormone-responsive |
| Key Molecular Alterations |
PTEN missense mutation (p.Glu288fs*3, p.Thr319fs*1); TP53 missense mutations (p.Asp49His, p.Met246Val); PI3K/Akt pathway activated; high microsatellite instability (MSI-H) |
| Additional Markers |
Expresses p160 steroid receptor coactivators (NCOA1-3); CD44 (hyaluronate receptor); SPP1; CD55; alkaline phosphatase responsive to estrogen stimulation |
| Karyotype |
Multiple severe karyotypic abnormalities; independent clonality confirmed |
| STR Profile |
Authenticated; Amelogenin: X; CSF1PO: 11,12; D13S317: 9,12; D16S539: 9; D18S51: 12,19; D19S433: 12.2,14; D21S11: 28; D2S1338: 20; D3S1358: 16,17; D5S818: 10,11; D7S820: 9,10; D8S1179: 13,16; FGA: 21; Penta D: 10,11; Penta E: 11,19.1; TH01: 9,10; TPOX: 8; vWA: 14,17 |
| Tumorigenicity |
Forms subcutaneous xenografts in immunodeficient mice (e.g., nude mice, NOD/SCID) when supplemented with estrogen; tumor growth typically measurable within 2-4 weeks |
| Culture Medium |
RPMI 1640 or DMEM supplemented with 10% fetal bovine serum (FBS) |
| ATCC Status |
Formerly CRL-2923; discontinued by ATCC due to reclassification concerns (reported as Ishikawa 3-H-12 derivative by some studies, though independent clonality has been supported by karyotype and p53 analysis) |
| Applications |
Preclinical evaluation of hormone therapies, PI3K/mTOR inhibitors, antiestrogenic agents, Wnt pathway modulators, and immunotherapy strategies in endometrial cancer |
Our Services
Alfa Cytology provides fully validated ECC-1 xenograft models with robust quality control at every stage---from cell line authentication and pathogen screening to in vivo tumor monitoring and endpoint histopathological analysis. Our platform supports flexible dosing regimens, combination therapy studies, and biomarker-driven endpoint collection, enabling you to generate reliable, publication-ready data for your endometrial cancer drug development programs. Partner with us to streamline your preclinical workflow and advance your therapeutic candidates with confidence.
Workflow of ECC-1 Xenograft Model Construction
The construction of the ECC-1 xenograft model follows a standardized, quality-controlled workflow designed to ensure reproducible tumor growth and reliable pharmacological readouts. Each stage incorporates rigorous validation criteria to maintain model integrity and data consistency across studies.
- Cell Line Preparation and Authentication: ECC-1 cells are expanded under standard culture conditions (RPMI 1640 or DMEM with 10% FBS) and authenticated via STR profiling prior to inoculation. Mycoplasma and pathogen screening are performed to ensure cell line purity. Cells are harvested at 80-90% confluence using gentle trypsinization, washed twice in sterile PBS, and resuspended at a concentration of 1 x 10^6 to 2 x 10^6 cells per 100-200 microL in a 1:1 mixture of serum-free medium and Matrigel to enhance engraftment efficiency.
- Mouse Strain Selection and Preparation: Immunodeficient female mice (e.g., NOD/SCID, nude/NU-NU, or NSG) aged 4-6 weeks are selected to minimize rejection of human tumor cells. Ovariectomy is performed in some protocols to eliminate endogenous ovarian hormones, followed by sustained estrogen supplementation (e.g., estradiol pellets or injections) to support ECC-1 tumor growth, given the cell line's hormone-dependent characteristics.
- Tumor Cell Inoculation: The prepared ECC-1 cell suspension is injected subcutaneously into the flank or mammary fat pad of anesthetized mice using a sterile 25-27 gauge needle. Typical inoculum volume ranges from 100-200 microL per site. Mice are monitored during recovery and returned to standard housing with controlled temperature (22 +/- 1 degrees C), humidity (55 +/- 5%), and a 12-hour light/dark cycle.
- Tumor Monitoring and Randomization: Tumor growth is monitored by palpation and caliper measurement every 3-5 days starting from day 7-10 post-inoculation. Tumor volume is calculated using the modified ellipsoid formula (V = 0.5 x length x width^2). Once tumors reach 100-200 mm^3, mice are randomized into treatment and control groups to ensure balanced baseline tumor volumes across cohorts.
- Treatment Administration and In-Life Observations: Test compounds are administered via the designated route (oral gavage, intraperitoneal, intravenous, or subcutaneous) according to the study protocol. Body weight, tumor dimensions, and clinical signs are recorded at regular intervals. Blood samples may be collected at predefined timepoints for pharmacokinetic or biomarker analysis.
- Endpoint Analysis and Necropsy: At study termination, tumors are excised, weighed, and processed for downstream analysis. Standard endpoints include tumor growth inhibition (TGI), tumor weight, and histopathological evaluation (H&E staining). Additional analyses such as immunohistochemistry (IHC) for Ki-67, ER, PR, p-AKT, cleaved caspase-3, or TUNEL assay for apoptosis may be performed based on study objectives.
- Data Compilation and Reporting: All raw data---including tumor growth curves, body weight trajectories, individual animal records, and histopathology images---are compiled into a comprehensive study report with statistical analysis (e.g., two-way ANOVA with repeated measures) to support regulatory and publication requirements.
Figure 2: Schematic workflow illustrating the derivation and construction of the ECC-1 Xenograft Model at Alfa Cytology.
Case Study-ECC-1 Xenograft Model Development
In a representative preclinical study, the ECC-1 xenograft model was successfully established in ovariectomized immunodeficient mice supplemented with exogenous estrogen. Subcutaneous inoculation of 1 x 10^6 ECC-1 cells in a Matrigel matrix resulted in consistent tumor formation within 14-21 days, with tumors reaching an average volume of 500-800 mm^3 by day 35. The established model demonstrated stable tumor growth kinetics suitable for therapeutic intervention studies. Treatment with a candidate PI3K inhibitor resulted in measurable tumor growth inhibition compared to vehicle controls, with corresponding reductions in Ki-67 proliferation index and p-AKT immunohistochemical staining in treated tumor tissues. These findings validated the ECC-1 xenograft as a responsive platform for evaluating targeted agents in hormone-driven endometrial cancer. Specific quantitative data and treatment arms can be customized to align with your compound's mechanism of action and study design requirements.

Why Choose Alfa Cytology?
Alfa Cytology delivers end-to-end preclinical oncology services with a focus on scientific rigor, operational flexibility, and client collaboration. Our ECC-1 xenograft model service is built on validated protocols and stringent quality standards to ensure data integrity and reproducibility.
- Validated Cell Line Authentication: All ECC-1 cells are STR-profiled and mycoplasma-tested prior to study initiation to guarantee model fidelity and prevent cross-contamination.
- Hormone-Optimized Model Conditions: We customize estrogen supplementation protocols to match the hormone-responsive nature of ECC-1, ensuring robust and consistent tumor engraftment rates.
- Comprehensive Endpoint Portfolio: From standard tumor growth inhibition and body weight monitoring to advanced IHC, biomarker quantification, and pharmacokinetic sampling, we offer flexible endpoint packages tailored to your study goals.
- Experienced In Vivo Team: Our scientists have extensive expertise in endometrial cancer xenograft construction, including orthotopic and heterotopic implantation techniques, with a track record of successful model delivery for diverse therapeutic modalities.
- Regulatory-Ready Documentation: Study reports are prepared in compliance with preclinical data standards, supporting IND-enabling studies, grant applications, and peer-reviewed publications with full traceability and statistical rigor.
- Rapid Study Turnaround: With established SOPs and dedicated project management, we offer competitive timelines from protocol design to final report delivery, accelerating your preclinical decision-making.
Contact Us
Ready to advance your endometrial cancer preclinical program with a validated ECC-1 xenograft model? Contact us today to discuss your study requirements, receive a customized protocol proposal, and learn how Alfa Cytology can accelerate your drug development timeline. Our team is standing by to reach out to you with expert guidance and tailored solutions for your next oncology project.
Reference
- Montero-Calle, Ana, et al. "In-depth quantitative proteomics analysis revealed C1GALT1 depletion in ECC-1 cells mimics an aggressive endometrial cancer phenotype observed in cancer patients with low C1GALT1 expression." Cellular Oncology 46.3 (2023): 697-715.
For research use only. Not intended for any clinical use.