KAT2B Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal carcinoma cell line HCT 116. This product provides a loss-of-function model for the gene encoding lysine acetyltransferase 2B (KAT2B, also known as PCAF), enabling investigation of histone acetylation-dependent transcriptional regulation and related signaling networks. The polyclonal pool preserves genetic heterogeneity and facilitates studies where clonal variation may be informative.
HCT 116 is a widely used epithelial colorectal carcinoma cell line established from a male patient. The cells exhibit microsatellite instability (MSI) and harbor oncogenic mutations in KRAS and CTNNB1 (??-catenin), along with other cancer-relevant genetic alterations. This genetic background makes HCT 116 particularly suitable for dissecting pathways involved in tumorigenesis, apoptosis, and DNA damage responses.
KAT2B functions as a histone acetyltransferase (HAT) that catalyzes acetylation of histones H3 and H4, as well as non-histone substrates, thereby modulating chromatin structure and gene expression. The protein acts as a transcriptional coactivator for several key regulators, including p53, E2F1, and SMAD3. KAT2B is activated by p53 and DNA damage stimuli, and it interacts with p300/CBP, ??-catenin, and PCAF-associated factor 65??. Downstream, KAT2B acetylates and influences the activity of targets such as p21/WAF1, c-Myc, cyclin D1, Bcl-2, MMP-2, and c-MET. Through these interactions, KAT2B integrates signals from p53, TGF-??, Wnt, and cell cycle pathways, regulating cell cycle arrest, apoptosis, and DNA repair.
In the HCT 116 background, disruption of KAT2B is expected to impair acetylation-dependent transcriptional programs that normally restrain tumorigenic properties. Because HCT 116 cells already contain activating mutations in ??-catenin and KRAS, loss of KAT2B may further dysregulate the KAT2B/??-catenin/TCF transcriptional complex and the p53/KAT2B/p21 axis, potentially affecting proliferation, survival, and migration. This knockout model thus provides a powerful tool to dissect KAT2B-dependent and -independent signaling nodes in a colorectal cancer context, and to evaluate the functional interplay between histone acetyltransferase activity and oncogenic driver mutations.
Applications include cancer biology, epigenetics, and signal transduction research, as well as drug resistance studies. Researchers can employ Western blotting to assess acetylation of histones H3/H4 and KAT2B target proteins, RT-qPCR for p21, c-Myc, and cyclin D1 expression, and ChIP-qPCR to examine histone acetylation at gene promoters. Flow cytometry enables cell cycle and apoptosis analysis, while migration and colony formation assays evaluate metastatic potential. Luciferase reporter assays can measure p53 and E2F1 transcriptional activity. These cells support investigation of DNA damage responses and TGF-??/Wnt signaling crosstalk. For further information, please contact Ascent Research.
