The ID3 Knockout NCI-H1703 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered for the targeted disruption of the ID3 gene in the human NCI-H1703 cell line. This product is supplied as a heterogeneous pool of cells, each carrying gene-editing events introduced by CRISPR/Cas9-mediated genome modification, resulting in loss-of-function of ID3. The polyclonal format preserves population diversity and avoids clonal selection biases, making it well-suited for studies requiring a representative knockout model. As a research-grade reagent, these cells are intended for in vitro functional investigations of ID3 in a lung squamous cell carcinoma background.
The host cell line, NCI-H1703, is a well-characterized non-small cell lung cancer (NSCLC) cell line derived from a human lung squamous cell carcinoma. It serves as a widely used model system for the study of squamous cell carcinoma biology, including proliferation, invasion, and drug response. NCI-H1703 cells exhibit typical molecular features of squamous cell carcinomas and are often employed in xenograft tumorigenicity assays and signaling pathway analyses. Their epithelial origin and genetic background make them particularly relevant for exploring the contribution of transcriptional regulators like ID3 to squamous cell carcinoma pathogenesis.
ID3 functions as a dominant-negative inhibitor of basic helix-loop-helix (bHLH) transcription factors, primarily by forming inactive heterodimers with E-proteins such as TCF3 (E2A), TCF4, and TCF12 (HEB), thereby preventing their DNA binding and transcriptional activation. ID3 expression is activated by BMP2/BMP4 and TGF-beta signaling through SMAD1/5/8, and is also regulated by MYC. It directly antagonizes the activity of bHLH factors that transcriptionally promote expression of cell cycle regulator CDKN1A (p21) and repress CCND1 (cyclin D1). Thus, ID3 controls the balance between proliferation and differentiation by modulating the transcriptional output of bHLH?CE-protein complexes, integrating inputs from BMP, TGF-beta, and Notch pathways to influence cell fate decisions.
In the NCI-H1703 context, disruption of ID3 is expected to relieve its repressive effects on bHLH-mediated transcription, potentially derepressing target genes such as CDKN1A and altering cyclin D1 levels. This derepression may restore aspects of cell cycle arrest or differentiation programs that are otherwise silenced in squamous carcinoma cells. Consequently, the ID3 knockout model provides a powerful tool to dissect how ID3 contributes to the malignant phenotype, including uncontrolled proliferation and evasion of differentiation. It also enables investigation of crosstalk between BMP/TGF-beta signaling and bHLH transcriptional networks in lung cancer.
Typical research applications for these polyclonal knockout cells include functional analyses of ID3 in lung squamous cell carcinoma, cell proliferation assays (e.g., MTT assay), drug resistance studies, differentiation analyses, and tumorigenicity assays. They are compatible with standard techniques such as western blotting, RT-qPCR, flow cytometry for cell cycle and apoptosis assessment, and transwell migration assays. By deploying this model, researchers can interrogate the mechanistic roles of ID3 in NSCLC and evaluate its potential as a therapeutic target. For further information or to discuss how this product can support your research, please contact Ascent Research.
