IL27 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human osteosarcoma cell line 143B. This product features targeted disruption of the IL27 gene via CRISPR/Cas9-mediated gene editing, resulting in a loss-of-function model that eliminates IL27 cytokine production. The polyclonal format provides a heterogeneous pool of knockout cells, representing a variety of editing events across the cell population, and is suitable for establishing stable knockout cultures for downstream functional analyses.
The parental cell line, 143B, is a widely characterized human osteosarcoma line derived as a subclone of HOS (human osteosarcoma). It is commonly employed in bone biology and oncology studies, particularly for investigating mechanisms of bone tumorigenesis, osteolytic bone destruction, and metastasis. The 143B cell line retains osteoblastic features and is highly tumorigenic in vivo, making it a robust model for both in vitro and in vivo bone cancer research.
IL27 encodes a heterodimeric cytokine belonging to the IL-12 family, composed of the EBI3 and p28 subunits. This cytokine exerts pleiotropic immunomodulatory effects, including promotion of Th1 cell differentiation and suppression of Th17 responses, through engagement of its receptor complex IL27RA/gp130. Downstream signaling is mediated via JAK1, JAK2, and TYK2 kinases, leading to phosphorylation and activation of STAT1 and STAT3 transcription factors, which in turn regulate genes such as T-bet, SOCS1, and SOCS3. Upstream regulation of IL27 expression is driven by TLR4 ligands, CD40L, IFN-gamma, and IL-1beta. Thus, IL27 functions at the intersection of innate and adaptive immunity, with critical roles in the JAK-STAT signaling pathway, Th1/Th2 cell differentiation, and inflammatory responses.
In the context of 143B osteosarcoma cells, IL27 knockout provides a defined system to dissect how tumor-derived IL27 influences the tumor microenvironment. Loss of IL27 production abrogates autocrine and paracrine JAK-STAT signaling, potentially altering immune cell recruitment, polarization, and anti-tumor immunity. This model is particularly relevant for studying osteosarcoma metastasis to bone, where cytokine crosstalk between tumor cells and bone-residing immune cells is pivotal. By eliminating IL27, researchers can investigate its contributions to tumor-immune crosstalk and the balance between pro- and anti-inflammatory signals within the bone niche.
This polyclonal knockout cell population is ideal for a variety of advanced research applications, including cytokine signaling studies, tumor-immune microenvironment characterization, osteosarcoma metastasis investigation, and functional genomics of IL27. Representative experimental assays include quantitative RT-qPCR for IL27 mRNA expression to confirm knockout, ELISA for secreted IL27 protein, Western blot analysis of STAT1/STAT3 phosphorylation, STAT-dependent dual-luciferase reporter assays for pathway activity, and co-culture assays with immune cells to assess functional outcomes. For further product information or technical support, please contact Ascent Research.
