The IL27 Knockout NCI-H1703 Polyclonal Cells comprise a heterogeneous population of the human lung squamous cell carcinoma line NCI-H1703 in which the IL27 gene has been disrupted via CRISPR/Cas9-mediated genome editing. This polyclonal format represents a pooled knockout population rather than a single-cell-derived clone, preserving the inherent genetic diversity of the parental line while ablating functional IL-27 cytokine expression. The product is designed as a loss-of-function model for investigating IL-27 biology in a squamous lung carcinoma background, enabling robust and reproducible experiments without clonal selection bias.
NCI-H1703 is a well-characterized cell line derived from a human squamous cell lung carcinoma, widely employed as a model system for non-small cell lung cancer (NSCLC). This adherent epithelial line retains key molecular features of lung squamous cancers, including relevant oncogenic and tumor suppressor gene alterations. It serves as a standard platform for studying tumor cell-intrinsic signaling, drug response, and interactions with the immune microenvironment, making it a relevant host for targeted gene knockout in immuno-oncology research.
IL-27 is a heterodimeric cytokine belonging to the IL-12 family, composed of EBI3 and p28 subunits. It signals through a heterodimeric receptor comprising IL27RA and gp130, activating JAK1 and downstream STAT1/STAT3. IL-27 is predominantly produced by antigen-presenting cells in response to stimuli such as TLR ligands, IFN-gamma, CD40 ligand, and LPS. Its signaling promotes Th1 differentiation while suppressing Th17 and regulatory T cell responses, mediated by induction of T-bet and effectors like Granzyme B and IL-10, with feedback inhibition via SOCS3. This network integrates JAK-STAT and NF-??B pathways.
In the context of NCI-H1703 lung squamous carcinoma cells, IL-27 signaling may influence tumor-intrinsic properties and the tumor-immune interface. Although IL-27 is primarily considered an immune cell-derived factor, its receptor components are expressed on various cell types, and autocrine or paracrine loops could modulate cancer cell behavior. This knockout model enables dissection of IL-27-dependent effects within the tumor cell compartment, independent of immune cell-derived cytokine. It provides a cleaner system for assessing how loss of IL-27 in the tumor microenvironment reshapes anti-tumor immunity and response to checkpoint blockade.
These polyclonal knockout cells are suited for diverse applications. They enable investigation of IL-27 in lung cancer immune evasion through tumor-immune coculture, using flow cytometry for T cell activation markers and multiplex bead arrays for cytokine profiling. As a screening platform, they support modulator studies with readouts like phospho-STAT1/STAT3 Western blotting and RT-qPCR for SOCS3/IL-10. They also facilitate checkpoint blockade response experiments in a defined genetic background. For further information, contact Ascent Research.
