The ART1 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the ART1 gene in the NCI-H1703 human lung squamous cell carcinoma line. This product provides a heterogeneous loss-of-function model to investigate ART1-dependent mono-ADP-ribosylation without clonal selection, preserving population-level diversity and minimizing artifacts associated with single-cell cloning. The polyclonal format is suitable for applications requiring faithful representation of parental cell biology.
The NCI-H1703 cell line represents a widely characterized model of non-small cell lung carcinoma, specifically derived from a squamous cell carcinoma. These epithelial cells exhibit hallmark features of advanced lung cancer, including aberrant integrin signaling, altered adhesion, and immune microenvironment interactions. The host background is ideal for exploring how post-translational modifications such as mono-ADP-ribosylation contribute to tumor progression and immune evasion in squamous cell lung cancer.
ART1 encodes a mono-ADP-ribosyltransferase that catalyzes the transfer of a single ADP-ribose moiety from NAD+ onto arginine residues on substrate proteins, of which integrin ??7 is a key target. This modification is induced downstream of pro-inflammatory cytokines through the transcription factors STAT3 and NF-??B, linking ART1 activity to inflammatory signaling. Upon upregulation, ART1-mediated mono-ADP-ribosylation of integrin ??7 alters its conformation and association with extracellular matrix, leading to attenuation of focal adhesion kinase (FAK) and Src kinase signaling, as well as altered Rho GTPase activity. Consequently, ART1 functions as a negative regulator of cell migration and a modulator of adhesion dynamics and immune regulatory processes.
In NCI-H1703 lung carcinoma cells, disruption of ART1 provides a powerful system to dissect the role of mono-ADP-ribosylation in tumor cell invasion, focal adhesion remodeling, and crosstalk with the microenvironment. Loss of ART1 is predicted to enhance integrin ??7-mediated adhesion signaling and migratory potential, enabling researchers to study how this post-translational modification influences squamous cell carcinoma aggressiveness. Additionally, the model permits investigation of ART1’s involvement in immune response modulation within the lung cancer setting, relevant to inflammatory aspects of tumor biology.
Researchers can employ these polyclonal knockout cells in a variety of experimental paradigms, including ADP-ribosylation activity assays, western blotting, RT-qPCR, migration and invasion assays, flow cytometry for integrin ??7, co-immunoprecipitation, and immunofluorescence. The model supports mechanistic studies of integrin signaling, post-translational modification crosstalk, and tumor microenvironment modulation, as well as screening of ART1 inhibitors or upstream regulators. For further details, please contact Ascent Research.
