The DNPH1 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the DNPH1 gene has been disrupted in the human NCI-H1299 non-small cell lung carcinoma cell line. This polyclonal knockout product provides a genetically heterogeneous pool of cells carrying targeted disruptions, enabling loss-of-function studies without the clonal selection bias inherent in monoclonal lines. CRISPR/Cas9-mediated genome editing was used to introduce targeted modifications, resulting in population-wide depletion of functional DNPH1 protein.
NCI-H1299 is a human lung adenocarcinoma cell line derived from lymph node metastasis, widely used as a model system for non-small cell lung cancer (NSCLC) research. It is p53-deficient and exhibits characteristics of aggressive, metastatic adenocarcinoma, making it a relevant platform for studying oncogenic signaling, drug resistance, and gene function in a disease-relevant background. This cell line is particularly suited for proliferation, migration, and therapeutic response assays.
DNPH1 encodes a 2′-deoxynucleoside 5′-phosphate N-hydrolase that hydrolyzes deoxyribonucleoside monophosphates (dNMPs) to free nucleobases and ribose-5-phosphate, directly regulating intracellular dNTP pools. DNPH1 expression is transcriptionally activated by MYC and E2F1, linking its activity to proliferative signaling. The protein acts as a homodimer and interacts with nucleotide metabolism enzymes to modulate nucleotide salvage, thereby influencing DNA synthesis, replication fidelity, and cell cycle progression. Overexpression enhances dNTP supply and proliferation, while disruption can cause replication stress and genomic instability.
In NCI-H1299 cells, which harbor hyperactive MYC and E2F pathways, DNPH1 knockout provides a critical tool to examine the dependency of lung adenocarcinoma cells on nucleotide salvage metabolism. Loss of DNPH1 function is expected to deplete dNTP pools, impair DNA replication, and sensitize cells to genotoxic stress or inhibitors of de novo nucleotide synthesis. This polyclonal knockout model enables the study of how DNPH1 deficiency impacts proliferation, cell cycle distribution, and DNA damage responses in a heterogeneous tumor cell population.
This product is ideal for functional genomics studies, drug target validation, and nucleotide metabolism research in lung cancer. Applications include cell proliferation assays (MTT, colony formation), dNTP pool quantification, ??H2AX immunofluorescence for DNA damage, comet assay, apoptosis detection, and drug sensitivity screening. Western blotting and RT-qPCR verify target depletion. The polyclonal format offers robust phenotypes averaged across the edited population. For further information, please contact Ascent Research.
