The IL27 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the IL27 gene. This product consists of a heterogeneous pool of CAL-27 cells harboring targeted disruptions in the IL27 coding sequence, enabling investigation of IL27-dependent biological processes without selection for a single clonal genotype. The polyclonal format preserves genetic diversity while providing a robust model for studying gene function in a physiologically relevant cancer cell background.
The CAL-27 host cell line was originally established from a human squamous cell carcinoma of the tongue and exhibits characteristics of both epithelial keratinocytes and fibroblasts. Importantly, these cells are human papillomavirus (HPV)-negative, making them a valuable model for HPV-independent oral carcinogenesis. CAL-27 cells are widely used in cancer research due to their tumorigenic properties, invasive potential, and responsiveness to cytokine signaling, thus providing a relevant context for interrogating the role of the pro-inflammatory cytokine IL27.
IL27 is a member of the IL-12 family of cytokines that plays a pivotal role in regulating both Th1 and Th2 immune responses. Mechanistically, IL27 signals through a receptor complex that includes IL27RA. Upon ligand binding, the receptor-associated Janus kinases TYK2 and JAK1 are activated, leading to phosphorylation and nuclear translocation of STAT1 and subsequent induction of downstream targets such as SOCS3. The IL27 gene is itself regulated by upstream factors including IFNGR and IL27RA, forming feedback loops within the JAK-STAT signaling pathway. This intricate network positions IL27 as a central mediator linking innate and adaptive immunity.
In the context of the CAL-27 squamous cell carcinoma line, disruption of IL27 expression provides a powerful tool to dissect the cytokine’s contribution to tumor-associated inflammation, immune evasion, and the tumor microenvironment. Given the absence of HPV-driven oncogenic mechanisms, this model allows focused analysis of IL27-mediated signaling in a purely chemical-carcinogenesis or genetic-instability background. Researchers can explore how loss of IL27 impacts STAT1 activation, SOCS3 induction, and broader JAK-STAT pathway dynamics, shedding light on potential therapeutic targets in head and neck cancers and inflammatory diseases.
Typical applications of this polyclonal knockout pool include functional genomics, drug target validation, and mechanistic studies of cytokine signaling using assays such as western blotting, RT-qPCR, flow cytometry, ELISA, and cell-based functional assays. These cells enable experiments examining proliferation, apoptosis, migration, and cytokine production in the absence of IL27. For custom inquiries, technical support, or bulk ordering, please contact Ascent Research.
