LS513 Xenograft Model Overview
The LS513 xenograft model is derived from a human colorectal adenocarcinoma cell line initially isolated from a primary colon tumor of a 62-year-old male patient. This model is well-suited for preclinical studies of microsatellite-stable (MSS) colorectal cancer, particularly in evaluating drug efficacy and resistance mechanisms. LS513 xenografts maintain a well-differentiated epithelial phenotype and exhibit moderate tumorigenicity, making them a reliable platform for testing both standard-of-care chemotherapies and novel therapeutics targeting key signaling pathways. LS513’s stable growth kinetics and its utility in drug resistance studies make it an ideal candidate for investigating the role of epithelial signaling, metastasis suppression, and chemotherapy combination strategies in colorectal cancer treatment.
Request a Custom Quote for LS513 Xenograft ModelBiological and Molecular Characteristics
LS513 cells exhibit an epithelial monolayer morphology with tight cell–cell junctions and strong expression of E-cadherin, indicating intact epithelial differentiation. The cell line is microsatellite stable (MSS) and has a wild-type KRAS, BRAF, and NRAS profile, making it responsive to EGFR-targeted therapies such as cetuximab and panitumumab. TP53 is mutated, which leads to dysfunctional apoptotic signaling and impaired DNA damage response, making the model suitable for studying therapies that target DNA repair mechanisms or exploit synthetic lethality. LS513 also expresses moderate levels of carcinoembryonic antigen (CEA) and cytokeratin 20 (CK20), confirming its colorectal origin. Additionally, the Wnt/β-catenin signaling pathway is active in LS513 cells, with β-catenin localizing both in the cytoplasm and at the cell membrane. These molecular features provide a robust model for testing therapies targeting EGFR, Wnt signaling, and DNA repair pathways.
| Characteristic | LS513 Cell Line Profile |
|---|---|
| Tissue of Origin | Colorectal adenocarcinoma (primary) |
| KRAS/BRAF/NRAS Status | Wild-type |
| TP53 Status | Mutated |
| MSI Status | Microsatellite stable (MSS) |
| Differentiation Markers | CK20, CEA, E-cadherin |
| Wnt Signaling | Active, β-catenin cytoplasmic/membranous |
In Vivo Model Development and Tumorigenicity
LS513 xenografts are generated by subcutaneous injection of cultured cells into immunodeficient mouse strains, such as athymic nude or NOD/SCID mice. Tumor formation is reliable, with growth detectable within 7 to 10 days post-inoculation. Tumors typically reach volumes of 700–900 mm³ within 4 to 5 weeks. The growth rate is moderate but consistent, making this model suitable for extended studies evaluating the effects of chemotherapeutics, targeted therapies, and combination regimens. The model’s stable tumorigenicity and epithelial differentiation enable the testing of agents that require a defined cellular architecture and intact cellular signaling. LS513 xenografts are also valuable for studies of tumor recurrence and resistance following chemotherapy treatment.
Request a Custom Quote for LS513 Xenograft ModelHistopathology and Immunohistochemical Profile
Histological analysis of LS513 xenografts reveals moderately differentiated adenocarcinomas with glandular structures and minimal stromal desmoplasia. Hematoxylin and eosin (H&E) staining highlights the presence of well-polarized epithelial cells with basal nuclei and clear cytoplasm. Immunohistochemical staining confirms strong expression of epithelial markers such as CEA, CK20, and E-cadherin, validating the colorectal origin of the tumors. β-catenin shows both membrane and cytoplasmic localization, indicating active Wnt signaling. Mutant p53 is present in the tumor nuclei, reflecting the model’s loss of functional p53-mediated apoptotic control. The overall histological consistency, combined with a clear molecular profile, makes LS513 a reliable model for colorectal cancer research and drug testing.
Preclinical Applications and Drug Response
The LS513 xenograft model is particularly useful for evaluating therapeutic agents in microsatellite-stable colorectal cancer. The wild-type KRAS, BRAF, and NRAS background ensures the model’s responsiveness to EGFR inhibitors, such as cetuximab and panitumumab, making it an ideal platform for studying the effectiveness of these therapies in MSS colorectal cancer. The TP53 mutation also allows for the investigation of agents that target apoptotic signaling, such as DNA-damaging agents or inhibitors of the DNA damage response pathway. LS513 xenografts are also valuable for testing novel therapeutics that target the Wnt/β-catenin signaling pathway, as well as combination therapies that incorporate chemotherapy and targeted agents. The model’s predictable growth and stability make it suitable for long-term treatment regimens and the assessment of drug resistance over time.
Request This Model
To integrate the LS513 xenograft model into your colorectal cancer research program, contact our scientific team to discuss study objectives, model specifications, and access to this highly reproducible and well-characterized model system.
Request a Custom Quote for LS513 Xenograft Model