HMGB1 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1703 human lung squamous cell carcinoma line. This product offers a mixed pool of cells with targeted disruption of the HMGB1 gene, facilitating loss-of-function studies while avoiding clonal selection artifacts. The polyclonal format preserves population heterogeneity and enables robust HMGB1 protein reduction, making it ideal for bulk assays and high-throughput screening applications.
The NCI-H1703 cell line was originated from a primary lung squamous cell carcinoma of a 54-year-old male. It serves as a well-characterized in vitro model for non-small cell lung cancer (NSCLC), specifically squamous cell carcinoma. NCI-H1703 cells exhibit epithelial morphology and express relevant tumor markers, providing a physiologically relevant context for studying tumor progression, metastasis, and drug resistance.
HMGB1 is a nuclear DNA-binding protein that regulates transcription, DNA repair, and nucleosome structure. In response to stress or necrosis, it relocates to the extracellular space and functions as a damage-associated molecular pattern (DAMP), binding RAGE, TLR2, and TLR4. This triggers the MyD88-dependent NF-??B pathway and the RAGE-MAPK-PI3K/AKT cascade. Upstream stimuli such as LPS, TNF-??, IL-1??, hypoxia, and oxidative stress induce HMGB1 release, while downstream signaling leads to activation of NF-??B and MAPK, and expression of TNF-??, IL-6, MMP-9, and VEGF. The HMGB1-TLR4-MyD88-NF-??B and HMGB1-RAGE-MAPK-PI3K/AKT axes coordinate inflammatory and pro-survival responses.
In NCI-H1703 squamous carcinoma cells, HMGB1 contributes to tumor progression and the inflammatory microenvironment. Tumor or stromal cell-derived HMGB1 can enhance proliferation, invasion, and therapy resistance via autocrine/paracrine mechanisms. Knockout of HMGB1 in this polyclonal model allows dissection of its role in NF-??B-driven survival, MAPK-mediated migration, and the interplay between autophagy and apoptosis. This model is useful for studying DAMP signaling in lung squamous cell carcinoma and for evaluating HMGB1 as a therapeutic target.
Typical applications include western blotting and RT-qPCR for knockout confirmation, cell proliferation and transwell migration/invasion assays, NF-??B reporter assays, and cytokine ELISA. The model supports RNA-seq transcriptomics, ChIP-qPCR for DNA-binding analysis, and drug resistance studies. These cells are also suited for high-throughput screening of HMGB1 pathway inhibitors. For detailed product information and technical support, contact Ascent Research.
