The ABHD12 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from Huh-7 hepatocellular carcinoma cells, featuring disruption of the ABHD12 gene. This loss-of-function model enables investigation of ABHD12-dependent lipid signaling and metabolic regulation in a liver cancer context. The polyclonal nature captures a spectrum of editing outcomes without clonal selection biases, suitable for functional genomics studies.
The Huh-7 host line, from a well-differentiated human hepatocellular carcinoma, exhibits epithelial morphology and is widely used in hepatocellular carcinoma research, hepatitis C virus infection models, and hepatic drug metabolism studies. Its robust growth and expression of key metabolic enzymes provide a relevant background for analyzing ABHD12??s role in hepatic lipid homeostasis.
ABHD12 is an endoplasmic reticulum-resident serine hydrolase that catalyzes the hydrolysis of lysophosphatidylserine (lyso-PS), thereby limiting activation of the GPR34 and GPR174 receptors. It functions within endocannabinoid and glycerophospholipid metabolic networks, intersecting with enzymes such as MAGL and FAAH. ABHD12 expression is modulated by metabolic and inflammatory cues, and its deletion causes lyso-PS accumulation, which can amplify GPR34-mediated signaling and dysregulate cell survival, proliferation, and inflammatory responses.
In hepatocellular carcinoma, ABHD12 knockout in Huh-7 cells provides a tool to examine how altered lyso-PS and endocannabinoid signaling influence cancer phenotypes. Hepatocarcinomas often reprogram lipid metabolism, and ABHD12 disruption may reveal vulnerabilities related to lipid mediator signaling. Additionally, as loss-of-function ABHD12 mutations cause the neurodegenerative PHARC syndrome, this model offers a platform to study metabolic defects common to both syndromes, despite its hepatic origin. The interplay between lipid handling and oncogenic AKT/ERK pathways can be directly assessed.
This polyclonal knockout population is suited for applications such as mechanistic studies of PHARC syndrome, lipid-mediated signaling in liver cancer, and metabolic phenotyping. Assays include western blotting for ABHD12, LC-MS/MS lyso-PS quantification, immunofluorescence for ER localization, viability and apoptosis assays, migration/invasion studies, lipid droplet staining, and phospho-signaling analysis (pERK, pAKT). For further information, contact Ascent Research.
