The ABHD6 Knockout HCT 116 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of HCT 116 cells in which the ABHD6 gene has been disrupted, generating a versatile loss-of-function model. This polyclonal knockout configuration minimizes clonal selection bias and offers a robust system for functional studies of endocannabinoid signaling and lipid metabolism. These cells enable researchers to explore gene function without the need for single-cell clonal isolation.
The parental HCT 116 cell line is a human epithelial colorectal carcinoma model characterized by an oncogenic KRAS G13D mutation and mismatch repair deficiency due to MLH1 hypermethylation, leading to microsatellite instability (MSI). These genetic alterations are hallmarks of certain colorectal cancers and render the line highly valuable for investigating tumor cell biology, signal transduction, and drug responses. The adherent and epithelial nature also supports diverse in vitro assays.
ABHD6 encodes a monoacylglycerol lipase that hydrolyzes the endocannabinoid 2-arachidonoylglycerol (2-AG) to arachidonic acid and glycerol, thereby terminating signaling through cannabinoid receptors CB1 and CB2. Its activity is regulated by PPAR??, PPAR??, and insulin signaling, and it functionally interacts with MAGL and FAAH. The resultant arachidonic acid fuels COX-2/LOX-mediated synthesis of prostaglandins and leukotrienes, bridging endocannabinoid and inflammatory mediator pathways.
In HCT 116 cells, ABHD6 knockout elevates 2-AG levels, potentiating CB1/CB2 receptor activation and downstream signaling. Given the oncogenic KRAS and MSI background, this modulation may impact cell proliferation, migration, and inflammatory responses, providing a powerful system to dissect the interplay between endocannabinoid tone and colorectal cancer pathogenesis. The model is particularly suited for studying how lipid signals converge with oncogenic and inflammation-driven pathways.
This product is designed for applications in endocannabinoid biology, lipid metabolism, cancer signaling, and drug target validation for metabolic disorders, neuropathic pain, and colorectal cancer. Researchers can utilize assays such as Western blotting, RT-qPCR, LC-MS/MS-based 2-AG quantification, cAMP activation assays, cell proliferation (MTS/BrdU), wound healing migration, Annexin V apoptosis, lipidomics, and phospho-signaling (MAPK/AKT) analysis. For technical inquiries, please contact Ascent Research.
