The IL10RB Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of the IL10RB gene. Disruption of the target locus was achieved through CRISPR/Cas9-mediated gene editing in the SK-HEP-1 host cell line, yielding a heterogeneous pool of cells carrying loss-of-function modifications in IL10RB. This knockout model enables researchers to dissect the roles of IL-10 receptor beta subunit signaling in a human hepatic adenocarcinoma background without the need for clonal isolation, facilitating robust population-level analyses.
SK-HEP-1 is a well-characterized cell line derived from the ascitic fluid of a patient with liver adenocarcinoma. It exhibits a hybrid endothelial-like and hepatic phenotype, expressing markers characteristic of liver sinusoidal endothelial cells and adenocarcinoma. The line is extensively used as a model for studying liver cancer biology, tumor?Cendothelial interactions, and cytokine signaling within the hepatic microenvironment. Its origin and properties make it a relevant host for investigating IL10RB-mediated pathways in liver malignancies.
IL10RB encodes the shared beta subunit required for receptor complexes of IL-10, IL-22, and type III interferons (IL-28, IL-29). Upon cytokine binding, IL10RB pairs with ligand-specific alpha chains, such as IL10RA for IL-10 or IL22RA1 for IL-22, and activates associated Janus kinases JAK1 and TYK2. These kinases phosphorylate signal transducer and activator of transcription 3 (STAT3) and, to a lesser extent, STAT1. Activated STAT3 translocates to the nucleus and promotes transcription of genes controlling cell survival (Bcl-2), proliferation (c-Myc, cyclin D1), and feedback inhibition (SOCS3). Thus, IL10RB is a critical node in anti-apoptotic, proliferative, and immune-modulatory pathways.
In the SK-HEP-1 model, knockout of IL10RB ablates IL-10- and IL-22-driven signaling, resulting in severely diminished STAT3 phosphorylation and loss of downstream target expression. This directly impairs the pro-survival and proliferative programs that support tumor growth and maintenance. Given the role of IL-10 and IL-22 in promoting an immunosuppressive tumor microenvironment and facilitating epithelial repair, this knockout model provides a powerful tool to examine how loss of IL10RB-dependent signals alters the malignant phenotype of liver adenocarcinoma cells and their crosstalk with immune cells.
This polyclonal knockout product is suitable for a range of experimental applications, including interrogation of JAK-STAT signaling dynamics, screening of IL-10/IL-22 receptor inhibitors, and functional assays of cell migration, invasion, and viability. Co-culture systems with immune cells can be employed to study tumor-immune interactions. Common downstream readouts include western blot detection of phosphorylated STAT3, RT-qPCR analysis of SOCS3 and Bcl-2 expression, and flow cytometry?Cbased phospho-STAT3 quantification. For further details, please contact Ascent Research.
