The A1BG Knockout NCI-H1703 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the A1BG gene in the NCI-H1703 human lung squamous cell carcinoma cell line. This polyclonal product provides a heterogeneous loss-of-function model suitable for functional studies without clonal isolation, enabling robust gene-function analysis in a physiologically relevant mixed population.
The NCI-H1703 cell line originates from a human lung squamous cell carcinoma, a major non-small cell lung cancer subtype. Retaining key genomic and phenotypic features of the original tumor, this adherent epithelial model is widely used to investigate squamous cell carcinoma biology, drug sensitivity, and tumor microenvironment interactions. The A1BG knockout in this background creates a disease-relevant system for dissecting gene function.
A1BG encodes a poorly characterized secreted glycoprotein of the immunoglobulin superfamily, implicated in immune modulation and cell adhesion. It is an acute phase protein regulated by IL-6, TNF-??, and glucocorticoids. Mechanistically, IL-6 activates JAK/STAT signaling, leading to STAT3 phosphorylation and nuclear translocation, where it partners with C/EBP transcription factors to drive A1BG expression. While downstream targets and binding partners remain undefined, the immunoglobulin domains likely mediate cell-cell interactions and immune complex formation.
In lung squamous cell carcinoma, A1BG may influence tumor progression by altering adhesion or immune evasion. Its knockout in NCI-H1703 cells permits direct interrogation of these roles, including responses to inflammatory cytokines, apoptotic stimuli, and chemotherapeutics. The polyclonal nature captures a spectrum of editing events, facilitating studies on functional heterogeneity and compensatory mechanisms.
Applications include proliferation, migration, and invasion assays to assess metastatic potential; apoptosis and flow cytometry analyses for programmed cell death and surface markers; RNA-seq for transcriptomic profiling; and xenograft tumor assays for in vivo tumorigenicity and drug response. Validation via Western blot and RT-qPCR confirms target disruption. For further details, please contact Ascent Research.
