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Colorectal cancer (CRC) animal model

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Model Introduction

Platform Service Advantages

Model Construction

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Colorectal cancer

Introduction to CRC Animal Models

Colorectal cancer (CRC) is the third most common malignancy worldwide, posing a serious threat to human health, with the highest incidence observed in the 40–50 age group. Therefore, establishing appropriate animal models of colorectal cancer is crucial for investigating the mechanisms underlying its initiation and progression, as well as for developing novel anti‑tumor therapeutics.

Advantages of Aniphe BioLab’s CRC Animal Model Platform Services

This platform boasts mature and comprehensive animal models for colorectal cancer (CRC), capable of meeting diverse research needs, including mechanistic studies, drug screening, and preclinical efficacy evaluation.

	The types of model construction are diverse. It encompasses mainstream models such as chemically induced models, cell‑inoculated CDX models, and tissue‑transplanted PDX models, catering to diverse research directions.
	High pathological fidelity It can simulate tumor proliferation, invasion, metastasis, and other processes, closely mimicking the pathological features of clinical colorectal cancer.
	The model exhibits strong stability. The modeling success rate is high, individual variability is minimal, experimental reproducibility is excellent, and the data are reliable.
	Standardized Feeding and Management All animals are raised under SPF-grade conditions, with continuous monitoring of their health status and a standardized, traceable experimental protocol.
	Comprehensive testing items Supports multi-dimensional testing, including pathology analysis, imaging, molecular biology, and tumor markers.
	End-to-end one-stop service Providing integrated services for model generation, animal husbandry and observation, sample collection, and biomarker analysis.

Tumor xenograft model

Currently, animal models of colorectal cancer xenografts are classified, based on the origin of the graft, into cell line–derived xenografts (CDX) and patient‑derived xenografts (PDX).

CDX is a model in which tumor cell lines are directly implanted into immunodeficient mice. This human‑derived xenograft model, established using tumor cell lines, is easy to perform, cost‑effective, and widely used in cancer research.

Aniphe BioLab’s Selected Cell Lines
Human-derived	HT-29, HCT-116, SW620
Mouse-derived	CT26, MC38

PDX models are established by implanting tumor tissue fragments derived from patients with colorectal cancer into immunodeficient mice. These PDX models faithfully recapitulate the histopathological features, oncogene expression profiles, and drug responses of the primary tumors, thereby exhibiting strong clinical predictive value.

Many patients with colorectal cancer die from liver metastases, as the liver is a common site of metastasis for colon cancer. Based on the site of transplantation, it can also be classified into heterotopic transplantation, such as splenic injection (for hepatic metastases).

Case Study: CT26 Splenic Liver Metastasis Model by Aniphe BioLab:

Method for Establishing a Splenic Liver Metastasis Model

Experimental animals: 5-week-old female BALB/c

Experimental Protocol:

Following anesthesia, a midline oblique incision was made in the upper abdomen of the mice. The spleen was carefully exteriorized and placed on a saline‑soaked gauze pad. Tumor cells were then slowly injected; once the splenic capsule became engorged and whitened, the spleen was repositioned, and the incision was closed with sterile sutures. Postoperatively, the animals were housed under SPF conditions. Following model establishment, the animals exhibited signs consistent with hepatic injury, thereby mimicking the clinical features of acute liver failure.

Experimental results

Weight measurement

Mice were weighed 2–3 times per week after vaccination, and no significant weight loss or emaciation was observed throughout the study period, indicating that, during the observation period, the model did not exhibit cachexia attributable to tumor progression, and the model demonstrated good tolerability.

Image source: Aniphe BioLab

In vivo imaging detection

Following vaccination, in vivo imaging was performed weekly, and analysis of the acquired images clearly revealed fluorescent signals in both the liver and spleen.

Image source: Aniphe BioLab

Photo at the finish line

Photographs taken at the endpoint reveal prominent masses in the liver and spleen, indicating successful engraftment and growth of the tumor both at the primary site and at metastatic sites, thereby confirming the successful establishment of the model.

Precautions

01 Approximately 10 days after cell injection, the tumors had already exhibited significant metastasis, indicating a short experimental duration.

02 This experiment must be conducted in a sterile environment, with animals housed in an SPF‑grade facility, and supplemented with appropriate antibiotics.

03 Inject an appropriate cell dose.

Splenocutaneous injection (for hepatic metastasis) predominantly induces liver metastases in colorectal cancer; the resulting model exhibits a phenotype that closely resembles the clinical features of postoperative liver metastases from colorectal cancer, making it widely used for investigating the mechanisms of hepatic metastasis and for screening drugs that inhibit liver metastasis.

Chemically induced model

Currently, commonly used chemical carcinogens for colon cancer include dimethylhydrazine (DMH), azoxymethane (AOM), and the inflammatory agent dextran sulfate sodium (DSS). These agents are relatively easy to prepare, exhibit good reproducibility, can be rapidly scaled up in large quantities, and broadly mimic the process of carcinogenesis, making them widely employed in experimental studies.

AOM/DSS–induced colorectal cancer model

Genetically engineered mice

Genetically engineered animal models of colorectal cancer are established by employing molecular biological techniques to edit genes implicated in the development of colorectal cancer, such as introducing exogenous oncogenes or knocking out endogenous tumor suppressor genes.

Hereditary Nonpolyposis Colorectal Cancer (HNPCC): HNPCC results from biallelic inactivation of the APC gene and mutations in mismatch repair genes (MLH1, MLH2, MSH6, PMS1, and PMS2). Homozygous knockout mice lacking either the MLH1 or MLH2 gene develop lymphoid neoplasms and are also predisposed to gastrointestinal tumors, making them an excellent model for studying HNPCC.

Familial adenomatous polyposis (FAP): Dysregulation of the Wnt signaling pathway, mediated by APC–β-catenin–TCF, is the primary mechanism underlying FAP. A point mutation at codon 850 in one allele of the APC gene gives rise to multiple intestinal adenomas, and mice carrying this mutation are known as Min (multiple intestinal neoplasia) mice, which are considered one of the most ideal experimental models for studying familial adenomatous polyposis (FAP).

Organoid model

Organoid models are generated by culturing stem cells or organ‑progenitor cells in vitro using 3D culture techniques, with targeted induction through the addition of specific extracellular matrix mimetics and cytokines, thereby yielding cellular tissues that closely resemble the architecture of their tissue of origin. As a novel research platform, organoids have opened new avenues for cancer research and offer unprecedented opportunities for precision oncology.