LS513 Xenograft Model Service for Colon Cancer

The LS513 Xenograft Model Service for Colon Cancer provides a robust preclinical platform for evaluating therapeutic efficacy in microsatellite-stable colorectal adenocarcinoma, leveraging a well-characterized epithelial cell line with wild-type RAS and active Wnt signaling pathways. At Alfa Cytology, we specialize in delivering high-quality, customized LS513 xenograft models tailored to your specific drug development pipeline, with comprehensive endpoint analysis and histopathological validation to accelerate your preclinical research objectives.
Overview of LS513 Xenograft Model for Colon Cancer
The LS513 cell line was established in 1985 from a primary mucin-secreting cecal adenocarcinoma biopsy obtained from a 63-year-old Caucasian male patient diagnosed with Dukes' C stage colorectal cancer. This cell line exhibits a near-diploid karyotype and maintains an epithelial monolayer morphology characterized by tight cell-cell junctions and strong E-cadherin expression, indicative of intact epithelial differentiation. LS513 is classified as microsatellite stable (MSS) and carries a heterozygous KRAS G12D mutation alongside wild-type BRAF and NRAS status, making it particularly relevant for studying EGFR-targeted therapies and RAS pathway inhibitors in the context of MSS colorectal cancer.
In xenograft applications, LS513 cells demonstrate reliable tumorigenicity when implanted subcutaneously into immunodeficient mouse strains such as athymic nude or NOD/SCID mice, with tumor formation typically detectable within 7 to 10 days post-inoculation. The model exhibits moderate but consistent growth kinetics, reaching tumor volumes of 700-900 mm^3 within 4 to 5 weeks. Histologically, LS513 xenografts form moderately differentiated adenocarcinomas with glandular structures, minimal stromal desmoplasia, and preserved expression of colorectal differentiation markers including carcinoembryonic antigen (CEA), cytokeratin 20 (CK20), and E-cadherin. The active Wnt/beta-catenin signaling pathway, with beta-catenin localizing in both cytoplasmic and membranous compartments, further enhances the model's utility for evaluating therapeutics targeting the Wnt cascade. Additionally, LS513 has been classified within the Consensus Molecular Subtype 3 (CMS3) category, exhibiting distinct caspase activation kinetics and apoptotic responses to combination chemotherapy regimens.
Figure 1. Effects of VD on the protein levels of Nox1 and p22-phox proteins in S513 cells. (Kikuchi, H, et al., 2025)
Cell Line Information: LS513
The following table provides comprehensive characterization data for the LS513 human colorectal carcinoma cell line, including genetic, molecular, and phenotypic features relevant to preclinical xenograft modeling.
| Characteristic |
Details |
| Cell Line Name |
LS513 (also LS-513, LS 513) |
| Accession / RRID |
CVCL_1386 |
| Tissue of Origin |
Colorectal adenocarcinoma, primary cecal tumor (ileocecal valve region) |
| Tumor Type |
Mucin-secreting cecal adenocarcinoma, Dukes' C stage |
| Patient Demographics |
63-year-old Caucasian male |
| Cell Type |
Epithelial |
| Growth Mode |
Adherent monolayer |
| Morphology |
Epithelial monolayer with tight cell-cell junctions |
| Doubling Time |
20-34 hours (literature-dependent) |
| Biosafety Level |
BSL-1 |
| Recommended Medium |
RPMI 1640 supplemented with 10% fetal bovine serum (FBS) |
| Culture Conditions |
37 degrees C, 5% CO2, humidified incubator |
| Microsatellite Instability Status |
Microsatellite Stable (MSS) |
| KRAS Status |
Heterozygous mutation: p.Gly12Asp (G12D) |
| BRAF Status |
Wild-type |
| NRAS Status |
Wild-type |
| TP53 Status |
Wild-type (reported in some studies; mutated in others --- verify with specific batch) |
| CTNNB1 (beta-catenin) Status |
Homozygous deletion: p.Ala5_Ala80del |
| Wnt Signaling |
Active; beta-catenin cytoplasmic and membranous localization |
| Differentiation Markers |
CEA (carcinoembryonic antigen), CK20 (cytokeratin 20), E-cadherin |
| Drug Transporters |
Expresses ABCB1 (P-gp), ABCC2 (MRP2), and ABCG2 (BCRP) |
| TGF-beta Response |
Well-characterized response to TGF-beta signaling |
| IGF Response |
Responsive to insulin-like growth factor (IGF) signaling |
| MACC1 Expression |
High expression of MET transcriptional regulator MACC1 |
| Consensus Molecular Subtype |
CMS3 |
| Tumorigenicity |
Reliable subcutaneous growth in nude mice; confirmed xenograft model |
| Tumor Growth Kinetics |
Tumor detectable 7-10 days post-injection; reaches 700-900 mm^3 in 4-5 weeks |
| Histopathology |
Moderately differentiated adenocarcinoma with glandular architecture |
| Stromal Features |
Minimal stromal desmoplasia |
| Applications |
EGFR inhibitor evaluation, chemotherapy response, Wnt pathway targeting, drug resistance studies, EMT research |
| Part of Collections |
AstraZeneca Colorectal Cell Line (AZCL) panel; NCI RAS program mutant KRAS panel; Cancer Dependency Map (DepMap); COSMIC cell lines project |
| Omics Data Available |
Deep exome, proteome, phosphoproteome, transcriptome (RNA-seq, microarray), DNA methylation, miRNA expression, phenotypic screen, shRNA library screening, SNP array |
| STR Profile |
Available via ATCC (CRL-2134), CLS (300457), KCLB (22134) |
| Mycoplasma Status |
Negative (verify with supplier certificate) |
| Storage |
Liquid nitrogen vapor phase |
| Shipping |
Dry ice |
Our Services
Alfa Cytology leverages decades of collective expertise in tumor model development to deliver validated LS513 xenograft systems that meet the rigorous demands of preclinical oncology research. Our platform integrates standardized cell culture protocols, quality-controlled inoculation procedures, and comprehensive endpoint analyses --- including tumor volume monitoring, body weight assessment, histopathological evaluation, and biomarker quantification --- to provide actionable data that supports your drug candidate's progression from bench to bedside. Whether you require single-agent efficacy studies, combination therapy evaluations, or mechanistic investigations into drug resistance and EMT pathways, our LS513 xenograft service offers a scientifically robust and operationally flexible solution.
Workflow of LS513 Xenograft Model Construction
The construction of LS513 xenograft models at Alfa Cytology follows a rigorous, standardized protocol designed to ensure reproducible tumor growth, consistent molecular profiles, and reliable pharmacological readouts. The workflow encompasses cell line authentication, in vitro expansion, immunodeficient host preparation, subcutaneous implantation, and longitudinal tumor monitoring, with each stage subjected to stringent quality control measures.
The detailed step-by-step workflow is outlined below:
- Cell Line Authentication and Quality Control: LS513 cells are authenticated via short tandem repeat (STR) profiling and confirmed mycoplasma-free before expansion. Genetic integrity is verified through targeted sequencing of KRAS, BRAF, and TP53 loci to ensure batch consistency with the expected MSS, KRAS G12D, wild-type BRAF molecular signature.
- In Vitro Cell Expansion and Harvesting: Authenticated LS513 cells are expanded in RPMI 1640 supplemented with 10% FBS under standard culture conditions (37 degrees C, 5% CO2). Upon reaching 70-80% confluence, cells are harvested using trypsin-EDTA detachment, washed in sterile PBS, and resuspended at a concentration of 5-10 x 10^6 cells per mL in serum-free medium containing 50% Matrigel for enhanced engraftment efficiency.
- Immunodeficient Host Preparation: Female athymic nude (nu/nu) or NOD/SCID mice aged 6-8 weeks are housed in specific pathogen-free (SPF) barrier facilities with controlled temperature, humidity, and light cycles. Animals undergo acclimatization for a minimum of 7 days prior to tumor cell inoculation, with baseline body weights and health status documented.
- Subcutaneous Tumor Cell Inoculation: LS513 cell suspensions (typically 5 x 10^6 cells in 100-200 microL volume) are injected subcutaneously into the right flank of each mouse using a sterile 1-mL syringe with a 25-gauge needle. The injection site is marked, and animals are monitored for immediate post-procedural recovery. Tumor formation is assessed by palpation beginning on day 7 post-inoculation.
- Tumor Monitoring and Endpoint Analysis: Tumor dimensions are measured twice weekly using digital calipers, and tumor volume is calculated via the modified ellipsoid formula (V = 0.5 x length x width^2). Body weights are recorded concurrently to assess treatment-related toxicity. Upon reaching predetermined endpoint criteria (typically 700-900 mm^3 or 4-5 weeks), tumors are excised, weighed, and processed for histopathological analysis (H&E, IHC for CEA/CK20/E-cadherin/beta-catenin), biomarker quantification, and molecular profiling.
Figure 2: Schematic workflow illustrating the derivation and construction of the LS513 Xenograft Model at Alfa Cytology.
Case Study-LS513 Xenograft Model Development
In a representative preclinical engagement, Alfa Cytology successfully established subcutaneous LS513 xenografts in athymic nude mice to evaluate the efficacy of a novel therapeutic candidate targeting the KRAS G12D mutation in combination with EGFR inhibition. Tumor-bearing animals were randomized into treatment and vehicle control cohorts upon reaching a mean tumor volume of approximately 150 mm^3. The study incorporated a multi-arm design encompassing monotherapy, combination therapy, and sequential dosing regimens, with tumor growth inhibition (TGI) and tumor growth delay (TGD) serving as primary efficacy endpoints. Secondary endpoints included histopathological assessment of tumor differentiation status, immunohistochemical quantification of proliferation (Ki-67) and apoptosis (cleaved caspase-3) markers, and pharmacokinetic profiling of the test compound. Detailed quantitative data, including individual animal tumor growth curves, survival analyses, and biomarker correlation matrices, are available upon request through direct consultation with our scientific team.

Why Choose Alfa Cytology?
Alfa Cytology distinguishes itself as a trusted partner in preclinical oncology research through a combination of scientific rigor, operational excellence, and client-centric service delivery. Our LS513 xenograft model service is built upon the following core competencies:
- Validated cell line sourcing and authentication via STR profiling, mycoplasma testing, and targeted mutational analysis to ensure genetic fidelity across all batches.
- Standardized xenograft protocols with documented standard operating procedures (SOPs) that guarantee reproducible tumor growth kinetics and consistent molecular phenotypes.
- Comprehensive endpoint analysis capabilities encompassing tumor volume monitoring, body weight assessment, histopathology (H&E, IHC), and biomarker quantification (ELISA, Western blot, flow cytometry).
- Flexible study designs accommodating single-agent efficacy, combination therapy, dose-response, and pharmacokinetic/pharmacodynamic (PK/PD) integration studies.
- Dedicated project management with regular progress reporting, real-time data access, and transparent communication throughout the study lifecycle.
- Competitive turnaround times and cost-effective pricing structures without compromising on scientific quality or regulatory compliance standards.
Contact Us
Ready to advance your colon cancer therapeutic program with a validated LS513 xenograft model? Reach out to our team today to discuss your specific study requirements, request a custom quote, or schedule a scientific consultation. We are committed to delivering preclinical data that accelerates your decision-making and strengthens your regulatory submissions.
Contact Alfa Cytology now to explore how our LS513 Xenograft Model Service for Colon Cancer can support your next-generation drug development pipeline.
Reference
- Kikuchi, Hidehiko, Sumiko Akiyoshi, and Harishkumar Madhyastha. "1alpha, 25-Dihydroxyvitamin D3 enhances Nox1 superoxide-generating activity of LS513 human colon cancer cells via up-regulating transcription of Nox1-related genes." Fundamental Toxicological Sciences 12.6 (2025): 165-171.
For research use only. Not intended for any clinical use.