HCT 116 p300 KO [F5] Cell Line
- Name Carlos Caldas
- Institute Cancer Research UK Cambridge Institute
Tool name: HCT 116 p300 KO [F5] Cell Line
Tool type: Cell Lines
Tool sub-type: Continuous
Parental cell line: HCT 116
Cancer type: Carcinoma
Growth properties: Adhesion properties; invasion; migration
Description: The HCT 116 p300 KO Cell Line is a tool for the in vitro study of p300 in colon carcinoma, and specifically of its role in p53-dependent apoptosis, cellular adhesion and migration. Cell lines available are p300 WT (HCT116), p300 KO Clone D10 (HCT116), p300 KO Clone F5 (HCT116), p300 KO Clone F2 (HCT116). Experiments conducted should be using at least 2 of the 3 KO cell lines. The best 2 KO clones are D10 and F5. Anyone requesting the cell line should use the parental cell line that the KOs were generated from. The p300 KO lines demonstrate an aggressive cancer phenotype in vitro, with loss of cell-cell adhesion, defects in cell-matrix adhesion, and increased migration through collagen matrices. p300 is a transcriptional cofactor involved in regulating multiple cellular processes including cell cycle regulation, proliferation, differentiation, apoptosis, DNA damage repair and adhesion properties. Somatic inactivating mutations of p300 are associated with several cancers including breast, colorectal and gastric cancers. CBP was not manipulated in this cell line
Research area: Cancer; Cell Cycle; Cell Structure and Motility; Drug Discovery & Development
Cellosaurus ID: CVCL_HG29
- For Research Use Only
- • ?-HPV 5 and 8 E6 disrupt homology dependent double strand break repair by attenuating BRCA1 and BRCA2 expression and foci formation.
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- • Metabolic consequences of p300 gene deletion in human colon cancer cells.
- • p300 is required for orderly G1/S transition in human cancer cells.
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- • Absence of p300 induces cellular phenotypic changes characteristic of epithelial to mesenchyme transition.
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- • p300 regulates p53-dependent apoptosis after DNA damage in colorectal cancer cells by modulation of PUMA/p21 levels.