Colon-26
1
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Colon-26 is a mouse colon adenocarcinoma cell line derived from the tumor tissue of Balb/c mice bearing Colon-26 carcinoma, induced by single rectal application of N-Nitroso-N-Methyl-urethan (NMU). Colon-26 should be cultured in RPMI1640 supplemented with 10% FBS, and the doubling time of Colon-26 is 15-20 hours.
Why choose Colon-26 from AcceGen?
Colon-26 from AcceGen has the best quality and has passeed an entire examination of quality control under the rigorous regulations and rules. Colon-26 is produced in Accegen’s world-class laboratory with standardized operating procedure. AcceGen supports colon-26 with safety packaging, high-speed delivery, and competitive price.
Species | Mouse |
Cat.No | ABC-TC0154 |
Product Category | Tumor Cell Lines |
Size/Quantity | 1 vial |
Shipping Info | Dry Ice |
Growth Conditions | 37 ℃, 5% CO2 |
Biosafety Level | 1 |
Storage | Liquid Nitrogen |
Product Type | Mouse Colon Cancer Cell Lines |
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FOR RESEARCH USE ONLY
The colon-26 cells were used to build the cachectic mouse model for the research of the cancer cachexia, which is a syndrome of progressive loss of skeletal muscle mass and adipose tissue, causing weight loss and weakness. After inoculation of colon-26 cells, the following syndromes were observed in the transplanted mice: the sustaining and extensive weight loss as tumor growth, hypoglycemia, hypercorticism, and disorders of hepatic functions. With the growth of colon-26 tumor, the skeletal muscle and adipose tissues were both progressively lost, and the muscle cross-sectional area and muscle strength were reduced. This depletion of muscle tissue, induced by the colon-26 tumor, might be involved in the activation of proteolytic systems of skeletal muscle. The cytokine IL-6 is essential but not entirely sufficient for causing cachexia. Hence, anti-IL-6 antibody can be considered as an effective way to prevent the weight loss induced by cachexia. Otherwise, colon-26 cell line can be used for metastasis studies. The injection of colon-26 cell line into the spleen of wild-type mice induced the expression of tumor necrosis factor alpha (TNF-alpha) and the formation of subsequent liver metastasis, which is possibly mediated by tumor necrosis factor receptor p55 signaling.