The DNPH1 Knockout NCI-H1703 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1703 human lung squamous cell carcinoma epithelial cell line. This product provides a loss-of-function model for the DNPH1 gene (encoding deoxynucleoside monophosphate hydrolase), enabling investigation of nucleotide salvage and oncogenic metabolic reprogramming. The polyclonal format offers a heterogeneous pool of edited cells, suitable for functional studies without single-cell cloning selection.
The host cell line NCI-H1703, established from a 54-year-old male patient with lung squamous cell carcinoma, exhibits adherent epithelial morphology and serves as a widely used model for studying lung squamous cell carcinoma biology. This cell line retains key features of the tumor microenvironment and is extensively employed in cancer cell biology, drug discovery, and therapeutic target validation.
DNPH1 encodes a deoxynucleoside monophosphate hydrolase that catalyzes the cleavage of dNMPs into deoxyribose 5-phosphate and free nucleobases, playing a critical role in regulating deoxyribonucleotide pools and supporting DNA synthesis. Expression of DNPH1 is transcriptionally regulated by the MYC proto-oncogene and E2F transcription factors, positioning it downstream of oncogenic signaling pathways that drive cell proliferation. Although direct interacting partners remain unknown, DNPH1 functionally integrates with pyrimidine salvage enzymes such as uridine-cytidine kinase (UCK) and uridine phosphorylase (UPP), influencing pyrimidine nucleoside salvage and downstream cell cycle progression.
Disruption of DNPH1 in NCI-H1703 cells provides a powerful tool to dissect the c-Myc-driven nucleotide metabolism axis in lung squamous cell carcinoma. This knockout model allows researchers to explore how loss of dNMP hydrolase activity impacts nucleotide pool homeostasis, DNA replication fidelity, and proliferative capacity in an epithelial tumor context. The model is particularly relevant for validating DNPH1 as a therapeutic target and for understanding metabolic vulnerabilities in c-Myc-overexpressing cancers.
This polyclonal knockout cell population is suitable for a broad range of applications, including confirmation of DNPH1 knockout by western blotting and RT-qPCR, cell proliferation assays (e.g., MTT, BrdU incorporation), cell cycle analysis by flow cytometry, and quantitative measurement of nucleotide pools via LC-MS. Additionally, the model supports transcriptome profiling by RNA-seq and drug sensitivity assays with nucleoside analogs to assess metabolic pathway dependencies. For further information, please contact Ascent Research.
