The IAH1 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, engineered to disrupt the IAH1 gene. This model leverages CRISPR/Cas9-mediated gene disruption to eliminate IAH1 protein function across a heterogeneous cell pool, providing a loss-of-function platform to investigate IAH1-dependent processes.
The parental HT29 cell line is a well-characterized model of colorectal adenocarcinoma, isolated from a primary tumor of a female patient. These epithelial cells harbor key oncogenic mutations, including BRAF V600E, APC, and TP53, which drive tumorigenic properties and aberrant signaling. HT29 cells are widely utilized in cancer research for their adherent growth, mucus-producing capacity, and utility in studying intestinal epithelial biology. Their well-defined genetic background makes them a useful host for dissecting gene function in the context of colorectal cancer metabolism.
IAH1 encodes a serine hydrolase with isoamyl acetate-hydrolyzing esterase activity, involved in lipid ester hydrolysis. The enzyme cleaves medium-chain fatty acid esters, releasing free fatty acids and alcohols that enter metabolic or signaling pathways. In the knockout model, disruption of IAH1 abolishes hydrolysis of isoamyl acetate and related substrates, likely perturbing intracellular lipid ester metabolism. This can alter pools of free fatty acids and coenzyme A derivatives, impacting energy production and lipid-mediated signaling. Key pathway components include IAH1, medium-chain fatty acid esters, free fatty acids, and coenzyme A derivatives.
In HT29 colorectal cancer cells, lipid metabolism is frequently reprogrammed to support proliferation and survival. Abolishing IAH1 activity provides a tool to examine the contribution of specific esterase-mediated hydrolysis to cancer cell metabolism. Disruption may affect tumor cell energetics, membrane biosynthesis, or signaling cascades dependent on lipid second messengers. This polyclonal knockout population enables investigation of how loss of IAH1 influences the metabolic adaptability of HT29 cells under diverse nutrient conditions.
The IAH1 Knockout HT29 Polyclonal Cells are suited for investigating IAH1 function in lipid metabolism, colorectal cancer metabolic reprogramming, and esterase substrate specificity. Typical assays include esterase activity measurement with para-nitrophenyl acetate, lipidomic profiling, cell proliferation assays, and soft agar colony formation to assess tumorigenicity. The model also supports drug metabolism research and fatty acid oxidation studies. For further details, please contact Ascent Research.
