The DNPH1 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting DNPH1 in the DLD-1 colorectal adenocarcinoma cell line. This pooled knockout model enables study of gene function without clonal selection, preserving cellular heterogeneity. It is designed for investigating purine nucleotide metabolism and its role in cancer.
DLD-1 is an epithelial cell line derived from a human colorectal adenocarcinoma, harboring mutations in APC, TP53, and KRAS. These alterations drive key oncogenic processes, making DLD-1 a widely used model for colorectal cancer research. The line??s genetic background provides a relevant context for assessing the impact of DNPH1 disruption on tumor cell biology.
DNPH1 hydrolyzes purine nucleosides into free purine bases and ribose-1-phosphate, channeling substrates into salvage pathways. The enzyme is transcriptionally regulated by c-Myc and operates downstream of this oncogene. Key pathway components include phosphoribosyl pyrophosphate (PRPP), hypoxanthine-guanine phosphoribosyltransferase (HGPRT), and adenine phosphoribosyltransferase (APRT). DNPH1 may interact with mitochondrial transporters and nucleoside-metabolizing enzymes, linking nucleoside catabolism to anabolic nucleotide synthesis.
In DLD-1 colorectal cancer cells, c-Myc-driven DNPH1 expression supports nucleotide pool maintenance, facilitating rapid proliferation. Disrupting DNPH1 in this model allows researchers to dissect the contribution of purine salvage to tumor metabolism, identify metabolic dependencies, and explore synthetic lethal interactions specific to colorectal cancer.
Applications include western blotting and RT-qPCR for knockout validation, purine nucleoside hydrolysis assays, proliferation (MTT, BrdU) and apoptosis studies, metabolomic profiling of nucleotide pools, and drug sensitivity testing with purine analogs. This polyclonal knockout population is a versatile resource for investigating c-Myc-dependent metabolic reprogramming and evaluating DNPH1 as a therapeutic target in colorectal cancer. For more information, contact Ascent Research.
