This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HCT 116 human colorectal carcinoma cell line, engineered to disrupt the BCHE gene encoding butyrylcholinesterase. The polyclonal format comprises a heterogeneous pool of cells with diverse editing outcomes, providing a robust loss-of-function model for studying BCHE-dependent processes without the confounding effects of clonal selection.
HCT 116 cells are epithelial cells isolated from a male colorectal carcinoma patient and are widely used as a model for colorectal cancer research. This cell line harbors an activating KRAS G13D mutation and a stabilizing CTNNB1 mutation, resulting in constitutive Wnt signaling, and exhibits microsatellite instability (MSI-high), reflecting DNA mismatch repair deficiency. These genetic features make HCT 116 particularly valuable for investigating tumor biology, drug responses, and oncogenic signaling pathways.
BCHE-encoded butyrylcholinesterase is a serine esterase that hydrolyzes choline esters such as acetylcholine and succinylcholine, playing a key role in cholinergic signaling termination and xenobiotic detoxification. Its expression is transcriptionally regulated by IL-6, glucocorticoid signaling, and Sp1, and it can be silenced via promoter methylation. BCHE activity produces choline and acetate, which modulate downstream effectors including muscarinic and nicotinic acetylcholine receptors, cell cycle regulators, and apoptosis effectors. Consequently, BCHE functions as a critical node linking cholinergic metabolism to cellular proliferation and drug sensitivity.
In the HCT 116 background, BCHE knockout disrupts butyrylcholinesterase activity, likely elevating local acetylcholine levels and sustaining cholinergic receptor activation. This perturbation can amplify cholinergic signaling, which in non-neuronal tissues such as colorectal carcinoma influences cell proliferation, apoptosis, and sensitivity to chemotherapeutic agents. Moreover, given HCT 116??s MSI-high status and KRAS/CTNNB1 mutations, BCHE disruption may further alter pathways relevant to tumor progression and drug metabolism, providing a unique tool to dissect the interplay between cholinergic signaling and colorectal cancer biology.
Researchers can employ this polyclonal knockout model to investigate BCHE function in colorectal cancer via a range of assays, including cholinesterase activity measurements, Western blotting for BCHE, RT-qPCR for transcript analysis, MTT cell viability tests, flow cytometry for cell cycle profiling, drug sensitivity testing, and migration assays. Typical applications encompass functional genomics of BCHE in colorectal cancer, drug metabolism and toxicity studies, cholinergic signaling in non-neuronal tissues, cancer cell proliferation assays, and biomarker validation. For further information, please contact Ascent Research.
