The HDHD2 Knouckout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma line. This product enables loss-of-function analysis of HDHD2, a gene encoding a putative haloacid dehalogenase-like hydrolase involved in nucleotide sugar metabolism. The polyclonal format provides a heterogeneous pool of edited cells, avoiding clonal selection artifacts and allowing robust assessment of HDHD2 function in cancer biology.
HT29 cells originate from a primary colorectal adenocarcinoma of a 44-year-old Caucasian female and are characterized by mutant p53 status and tumorigenic capacity. They serve as a well-established model of intestinal epithelial physiology, widely used for investigating colorectal cancer mechanisms, drug transport, and epithelial barrier function. The defined genetic background and stable growth properties make HT29 an ideal host for gene disruption studies.
HDHD2 belongs to the haloacid dehalogenase superfamily and is predicted to function as a phosphatase that dephosphorylates nucleotide sugars such as UDP-glucose, UDP-galactose, and CMP-sialic acid. Through this activity, HDHD2 regulates the availability of substrates for glycosyltransferases, thus influencing protein glycosylation and glycolipid synthesis. It operates within nucleotide sugar and pyrimidine metabolism pathways, interacting with metabolic enzymes and sharing sequence homology with related hydrolases HDHD1 and HDHD3. Loss of HDHD2 likely disrupts nucleotide sugar pools, with consequential effects on glycosylation-dependent signaling and cellular metabolism.
Disruption of HDHD2 in HT29 cells offers a powerful model to explore the role of nucleotide sugar metabolism in colorectal cancer. Given HT29??s reliance on altered metabolic pathways and glycosylation for proliferation and survival, HDHD2 knockout may reveal novel insights into energy metabolism, glycocalyx composition, and tumor cell invasiveness. This model is relevant to research on colorectal and hepatocellular carcinomas, as well as metabolic disorders linked to aberrant glycosylation.
The HDHD2 Knouckout HT29 Polyclonal Cells support a wide range of applications, including mechanistic studies using Western blotting, RT-qPCR, and phospho-signaling arrays to map downstream signaling changes. Functional assays such as cell viability, migration/invasion, and Seahorse metabolic profiling can quantify tumorigenic and metabolic phenotypes. Lectin staining and flow cytometry permit detailed analysis of glycosylation alterations and cell surface marker expression. This polyclonal knockout population is an invaluable tool for functional genomics, drug target validation, and therapeutic research in cancer metabolism. For inquiries or customized gene-editing services, please contact Ascent Research.
