IL27 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line. This product provides a heterogeneous pool of IL27-disrupted cells, enabling robust loss-of-function studies in a well-established epithelial cancer model. The polyclonal format preserves genetic diversity and avoids clonal selection bias, making it suitable for population-level functional screens and assays requiring representative cellular heterogeneity.
HeLa cells are a classic human epithelial cell line originally isolated from a cervical adenocarcinoma and are positive for human papillomavirus type 18 (HPV-18). They serve as a versatile host for investigating oncogenic signaling, viral?Chost interactions, and cytokine-mediated processes. Their rapid proliferation, ease of genetic manipulation, and extensive characterization make them an ideal background for CRISPR-based gene disruption studies focused on immunomodulatory targets.
IL27 encodes a heterodimeric cytokine composed of EBI3 and p28 subunits that signals through a receptor complex of IL27RA and gp130. Ligand binding activates associated Janus kinases JAK1, JAK2, and TYK2, leading to phosphorylation and nuclear translocation of STAT1 and STAT3. These transcription factors induce downstream effectors such as T-bet and IL-10 while also upregulating SOCS3 as a negative feedback regulator. The pathway is triggered by upstream stimuli including TLR4 ligands, IFN-gamma, and CD40 ligand, primarily via NF-??B activation. IL27 plays a pivotal role in balancing Th1 and Th2 differentiation, promoting IL-10-mediated anti-inflammatory responses, and modulating immune cell function.
In the HeLa epithelial context, disruption of IL27 allows dissection of its non-immune cell-intrinsic roles, particularly in tumor-intrinsic JAK-STAT signaling and cytokine crosstalk. Given HeLa??s HPV-18-positive status and its origin from a cervical tumor, this knockout model is valuable for exploring how loss of IL27 signaling influences cancer cell proliferation, survival, senescence, and the expression of immunomodulatory factors that shape the tumor microenvironment. Researchers can examine altered phosphorylation dynamics of STAT1 and STAT3, changes in IL-10 secretion, and modified responses to inflammatory stimuli.
Typical experimental applications include quantitative RT-qPCR to confirm loss of IL27 transcript, western blotting for EBI3 and p28 subunits, and phospho-STAT1/STAT3 analysis upon cytokine stimulation. IL-10 ELISA can be employed to assess functional output, and flow cytometry can monitor IL27RA surface expression. This model supports screens for immune checkpoint modulators, mechanistic studies of cytokine networks, and functional interrogation of the JAK-STAT pathway in a cancer context. For further information or technical support, please contact Ascent Research.
