KPC Cell Line (C57/BL6 genetic background)
Established cell line used as a model of pancreatic ductal adenocarcinoma.
Contributors
| Inventor | Institute |
|---|---|
| Jennifer Morton | Cancer Research UK, Glasgow Beatson Institute |
| Cat. #: | 153474 |
|---|---|
| Tool sub type: | Continuous |
| Unit size: | 1×10^6 cells / vial |
| Cancer types: | Pancreatic cancer |
| Research Fields: | Cancer;Drug development |
| Organism: | Mouse |
| Gender: | Male |
| Model: | Transgenic |
| Growth properties: | Loosely adherent |
| Cancer Types In Detail: | Pancreatic cancer ; Pancreatic ductal adenocarcinoma |
| Alternate name: | PDAC cell line |
|---|---|
| Product description: | This KPC cell line represents a useful model of pancreatic ductal adenocarcinoma. This cell line was established from a popular KPC mouse model (Hingorani et al. 2005). It is applicable for use with C57BL/6 mice. Details on source mouse model The KPC mice from which the KPC cell is derived, are an establish clinically relevant model of PDA, that develop many of the key features of observed in human PDA such as pancreatic intraepithelial neoplasia. The KPC mouse contains a conditional point mutation in the transformation related protein 53 gene (TP53R172H), and a point mutation in the KRAS gene (KRASG12D) both of which generate non-functional proteins. A lox-stop-lox termination sequence is encoded upstream of both mutated genes to prevent expression in the absence of Cre recombinase. PDX1 (pancreatic and duodenal homeobox 1) is a transcription factor necessary for pancreatic development. The PDX1 promoter enables expression of Cre recombinase in acini, islet and duct cells of the pancreas. Cre-mediated recombination excises the two lox-stop-lox termination sequences and enables expression of both oncogenes: KRASG12D and TP53R172H in pancreatic tissue. Tissues not expressing Cre recombinase remain functionally heterozygous of the KRAS and TRP53 loci. KPC cell line The KPC cell line was derived from a KPC model that has been backcrossed for 10 generations into C57/B6 genetic background. This cell line retains the mutations seen in the parental KPC murine model. This cell line has been used in orthotropic injections into C57BL/6 mice, generating models of PDA. This KPC model can be used for PDA modelling, biomarkers investigation, genetics, and metastasis studies as well as drug discovery and development. Our current stock of this model is derived from male mice. |
| Gender: | Male |
| Conditional: | No |
| Production details: | These cells are from the KPC mouse which has been backcrossed to F10 in C57/BL6. KPC Subtype: C57Bl6/J. Isolation of the cells: For each cell line, a 5mm diameter piece of tissue was harvested from solid PDAC arising in a C57BL/6 KPC mouse into DMEM. The tissue was chopped into a fine paste, resuspended in DMEM + L-Glut, Pen-Strep and 20% FBS, and plated out in a 25cm flask. The medium was changed after 2 days. Once confluent the cells were passaged as normal and grown in DMEM + L-Glut, Pen-Strep and 10% FBS in normoxic conditions at 37C in a humidified incubator |
| disease: | Cancer |
| Format: | Frozen |
|---|---|
| Storage conditions: | Liquid Nitrogen |
| Shipping conditions: | Dry ice |
| Growth medium: | High-glucose DMEM (4.5 g/L) containing 10% foetal bovine serum and 2 mM l-glutamine |
| Subculture routine: | Cells are loosely adherent but will need trypsinising. High-glucose DMEM (4.5 g/L) containing 10% foetal bovine serum and 2 mM l-glutamine with 5% CO2 and air. A 1:2 split can be made every two days which is relatively standard. Incubated as standard |
| Temperature: | 37 ° C |
| Atmosphere: | CO2 |
| Mycoplasma free: | Yes |
| Biosafety level: | 1 |
| References: |
Romac JMJ et al. 2025. JCI Insight. 10:e179028. PMID: 41100488 Ianniello A et al. 2025. Molecular Cancer. 24:62. PMID: 39808462 Go M et al. 2024. eLife. 13:RP100089. PMID: 39656086 Tintelnot J et al. 2023. Nature. 618:627–634. PMID: 37092916 Schwartz PB, Brandes RP, Ovsiannikova N, et al. 2023. PLOS Genetics. 19(6):e1010791. PMID: 37262074 Woeste MR et al. 2023. Cancers. 15(9):2463. PMID: 37072351 Falcone M et al. 2022. British Journal of Cancer. 127(8):1522–1536. PMID: 36115879 Frey N et al. 2022. Nature Communications. 13:6409. PMID: 35379808 Leijnse C et al. 2022. Nature Communications. 13:6716. PMID: 35347113 Geller A et al. 2022. Nature Communications. 13:3892. PMID: 35140221 Newman AC et al. 2021. Molecular Cell. 81(11):2290–2302.e7. PMID: 33831358 Rossi Sebastiano M et al. 2020. Sci Adv 6(44):eabb9200, PMID: 33127675 Michalopoulou E et al. 2020. Cell Reports. 30(8):2729–2742.e4. PMID: 32101748 Allen-Petersen BL et al. 2019. Cancer Research. 79(10):2517–2529. PMID: 30389701 |
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