IL27 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the LoVo human colorectal adenocarcinoma cell line. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption of the IL27 locus, resulting in ablation of the p28 subunit of interleukin-27. As a polyclonal pool, the product retains genetic diversity while collectively eliminating functional IL27 expression, providing a robust cellular background for studying IL-27-dependent signaling pathways without the limitations of single-cell clonal variation. Researchers can use these polyclonal knockout cells to interrogate the roles of IL-27 in tumor biology, immune modulation, and cytokine signal transduction with high biological relevance.
The host LoVo cell line is derived from a metastatic site of a Dukes’ type C colorectal adenocarcinoma, representing an epithelial-like cellular model that retains key characteristics of advanced colorectal cancer. This cell line is widely used to investigate metastatic mechanisms, adhesion, and tumor?Cmicroenvironment interactions. Its well-characterized genetic background and stable growth properties make it ideal for generating gene-edited derivatives. Because LoVo cells express components of the JAK-STAT signaling pathway and can respond to cytokines such as interferons and interleukins, they provide a physiologically relevant platform for dissecting IL-27-mediated signaling networks in the context of gastrointestinal malignancy.
IL27 encodes the p28 subunit, which dimerizes with Epstein-Barr virus-induced gene 3 (EBI3) to form the heterodimeric cytokine IL-27. Secreted IL-27 binds to a cell-surface receptor complex consisting of IL27RA (WSX-1) and gp130 (IL6ST), which recruits the Janus kinases JAK1 and TYK2. Ligand-induced receptor activation triggers phosphorylation of STAT1 and STAT3, leading to their nuclear translocation and transcriptional regulation of target genes such as TBX21 (T-bet), SOCS1, ICAM1, and CXCL10. This cascade is tightly controlled by upstream signals including TLR4 agonists, interferon gamma (IFNG), and NF-??B activation. IL-27 signaling promotes Th1 differentiation, suppresses Th17 and regulatory T cell responses, and contributes to anti-tumor immunity. Consequently, disruption of IL27 in LoVo cells eliminates the ability to produce p28, thereby preventing EBI3-p28 heterodimer assembly and downstream JAK-STAT signal transduction.
In the context of colorectal cancer, IL-27 has been implicated in shaping the tumor immune microenvironment and inhibiting tumor progression through STAT1- and STAT3-dependent mechanisms. By knocking out IL27 in LoVo cells, researchers can dissect the contribution of autocrine or paracrine IL-27 signaling to malignant phenotypes such as proliferation, migration, and invasion. This model also enables the investigation of how cancer cells may evade immune surveillance when the IL-27 axis is disrupted. Furthermore, the LoVo polyclonal knockout pool avoids clonal artifacts, allowing assessment of heterogeneous responses to cytokine stimulation or immune effector cells, which is especially relevant for studies that require population-level insights into colorectal cancer biology.
These polyclonal knockout cells support a wide range of experimental applications, including detailed analysis of IL27-mediated anti-tumor immunity, evaluation of cytokine signaling in colorectal cancer, dissection of immune checkpoint modulation, and investigation of STAT3-dependent gene regulatory networks. Representative assays that can be performed with this model include Western blotting for IL27 protein, RT-qPCR for IL27 mRNA, ELISA for secreted IL-27, flow cytometric analysis of IL27RA receptor expression, phospho-STAT1/STAT3 signaling assessments, co-culture immune cell activation assays, and functional assays measuring proliferation, migration, or invasion. For more information regarding the product and its applications, please contact Ascent Research.
