This product consists of a polyclonal population of SK-HEP-1 human hepatocellular carcinoma cells carrying a CRISPR/Cas9-mediated disruption of the ABHD12 gene. The resultant ABHD12 knockout polyclonal cells are supplied as a heterogeneous pool, enabling loss-of-function studies without clonal selection artifacts. As a gene-edited cell reagent, these polyclonal cells serve as a basis for investigating ABHD12-dependent processes in a liver cancer context.
The host cell line, SK-HEP-1, was originally established from the ascitic fluid of a patient with liver adenocarcinoma and is widely employed as a model for hepatocellular carcinoma (HCC) biology. This adherent cell line retains features relevant to hepatic drug metabolism and lipid handling, making it a suitable platform for examining the intersection of tumor cell physiology and lipid signaling. Its routine use in pharmacological and toxicological studies provides a well-characterized background for interpreting phenotypes arising from target gene disruption.
ABHD12 encodes a serine hydrolase that selectively hydrolyzes lysophosphatidylserine (lyso-PS), a bioactive lipid ligand of the G protein-coupled receptor GPR34. In resting cells, ABHD12 maintains low lyso-PS levels, thereby limiting GPR34-driven phagocytic signaling and immune activation. The enzyme is induced by inflammatory stimuli such as TNF-alpha and lipopolysaccharide (LPS) acting via Toll-like receptor pathways, positioning it at a regulatory node between inflammation and lipid mediator clearance. ABHD12 functionally interacts with its paralog ABHD12B and operates within the broader endocannabinoid system, where its activity influences the balance of pro- and anti-inflammatory lipid species. Disruption of ABHD12 leads to lyso-PS accumulation, sustained GPR34 activation, and downstream dysregulation of phagocytic function, which are central to the neuroinflammatory pathology observed in human PHARC syndrome (polyneuropathy, hearing loss, ataxia, retinitis pigmentosa, cataract).
In the SK-HEP-1 background, loss of ABHD12 allows direct examination of lyso-PS metabolism and GPR34 signaling in a cancer cell milieu. Hepatocellular carcinoma cells exhibit altered lipid metabolism, and the ABHD12 knockout model provides a tool to dissect how aberrant lysophospholipid turnover contributes to tumor-associated immune modulation, phagocytic clearance, and potentially drug resistance. Because SK-HEP-1 cells are responsive to lipid-related inflammatory cues, this polyclonal knockout population is particularly valuable for studying the crosstalk between endocannabinoid-regulated pathways and oncogenic processes in the liver.
Researchers can employ these knockout cells in a range of assays, including liquid chromatography?Cmass spectrometry (LC-MS) quantification of lyso-PS to confirm metabolic disruption, phagocytosis assays to assess immune-like functions, and immunoblotting or RT-qPCR for pathway validation. The cells are also compatible with immunofluorescence and flow cytometry for receptor trafficking or cell-surface marker analyses, as well as MTT and Annexin V apoptosis assays to evaluate proliferation and viability. Lipidomic profiling can further reveal broader changes in the lipidome linked to ABHD12 deletion. Altogether, this polyclonal ABHD12 knockout product offers a versatile platform for disease modeling, lipid signaling investigation, and drug target validation in hepatocarcinoma research. For additional details, technical support, or bulk ordering, please contact Ascent Research.
