The AGPS Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 colorectal adenocarcinoma cell line, in which the AGPS gene has been disrupted. This polyclonal mixture of edited cells provides a heterogeneous loss-of-function model for studying AGPS-dependent ether phospholipid biology in a human colorectal cancer context.
The HT29 cell line was originally established from the primary colorectal adenocarcinoma of a 44-year-old female and serves as a well-characterized model for intestinal epithelial biology and colorectal cancer. HT29 cells exhibit epithelial morphology and retain key features of intestinal differentiation, making them a valuable platform for investigating lipid metabolism, membrane dynamics, and oncogenic signaling pathways.
AGPS encodes alkylglycerone phosphate synthase, a peroxisomal enzyme that catalyzes the conversion of acyl-dihydroxyacetone phosphate (acyl-DHAP) to alkyl-DHAP, the rate-limiting step in ether phospholipid biosynthesis. This reaction is essential for the production of plasmalogens, including ethanolamine and choline plasmalogens, which are critical components of cellular membranes. AGPS functions within a network that includes GNPAT, FAR1, and the peroxisomal import receptors PEX5 and PEX7. Its activity is transcriptionally regulated by PPARA and SREBF1, linking ether lipid synthesis to broader metabolic and proliferative signals.
Disruption of AGPS in HT29 cells impairs plasmalogen production, leading to altered membrane lipid composition and potentially affecting membrane fluidity, signal transduction, and cellular responses relevant to colorectal cancer pathophysiology. This model enables the dissection of ether lipid contributions to cancer cell survival, migration, and drug resistance. It also supports studies of peroxisomal disorders such as rhizomelic chondrodysplasia punctata type 3 and Zellweger spectrum disorders, where AGPS deficiency plays a central role.
Researchers can employ this polyclonal knockout cell population in a range of experimental workflows, including lipidomics to quantify plasmalogen depletion, RT-qPCR and Western blotting to confirm loss of AGPS expression, and functional assays such as cell viability, migration, and apoptosis to assess phenotypic consequences. Additionally, immunofluorescence can be used to monitor peroxisomal integrity. This versatile tool is well-suited for mechanistic investigations into ether lipid-mediated signaling in colorectal cancer and for metabolic pathway analysis. For further information, please contact Ascent Research.
