The IL27 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in the human SK-HEP-1 cell line, designed for investigating IL27 function. This product features a targeted disruption of the IL27 gene, resulting in loss of functional IL27 cytokine production within a polyclonal cellular context. The polyclonal nature provides a heterogeneous population that more closely mimics in vivo genetic variability, avoiding clonal artifacts. The CRISPR/Cas9-mediated gene knockout offers a stable loss-of-function model without the need for continuous drug selection, enabling robust downstream phenotypic analyses.
The SK-HEP-1 cell line, derived from the ascites of a patient with hepatic adenocarcinoma, displays an endothelial-like phenotype and is widely utilized as a model for liver biology and hepatocellular carcinoma. These cells retain key metabolic and secretory functions characteristic of liver parenchyma, making them suitable for studying hepatocyte-derived cytokine signaling and tumor?Cstroma interactions. SK-HEP-1 cells express components of the JAK-STAT pathway and respond to various inflammatory stimuli, providing a versatile platform for dissecting cytokine networks in a hepatocellular carcinoma context.
IL27 is a pleiotropic cytokine of the IL-12 family that signals through a heterodimeric receptor composed of IL27RA and gp130, activating JAK1 and TYK2 kinases to phosphorylate STAT1 and STAT3. Critical downstream mediators include T-bet, PD-L1, and the anti-inflammatory cytokine IL-10, while SOCS3 functions as a negative feedback regulator. IL27 expression is stimulated by TLR agonists (LPS, CpG), IFN-gamma, and CD40L, integrating innate and adaptive signals. This cytokine modulates Th1, Th2, and Th17 differentiation, influencing both pro-inflammatory and regulatory programs in the tumor microenvironment.
In SK-HEP-1 cells, disruption of IL27 provides a valuable tool to dissect hepatocellular carcinoma biology and tumor-immune crosstalk. Loss of autocrine IL27 signaling may alter expression of PD-L1 and SOCS3 and modulate STAT1/STAT3 activity. This model enables investigation of how hepatic tumor cells contribute to immune evasion, cytokine milieu remodeling, and T cell response regulation. It also permits exploration of IL27-dependent effects on proliferation, migration, and invasion, relevant to metastatic progression.
This polyclonal knockout cell product is suitable for a range of experimental applications, including cancer immunology, tumor microenvironment studies, cytokine signaling dissection, and drug screening. Representative assays include western blotting and RT-qPCR to confirm IL27 disruption, ELISA for secreted IL27 quantification, phospho-STAT1/3 flow cytometry to assess pathway activation, co-culture systems with immune cells to evaluate functional interactions, and PD-L1 immunofluorescence to gauge checkpoint molecule expression. Proliferation, migration, and invasion assays can further delineate phenotypic consequences. For detailed technical specifications or assistance, please contact Ascent Research.
