The IL27 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from A-549 cells, featuring targeted disruption of the IL27 gene. This product provides a heterogeneous pool of cells carrying loss-of-function mutations in IL27, enabling functional studies of interleukin-27 deficiency without the need for clonal isolation. The polyclonal format retains the genetic diversity of the knockout population, reflecting a more physiologically relevant model for bulk population-level analyses.
The parental A-549 cell line originates from human lung adenocarcinoma tissue of a 58-year-old male and exhibits characteristics of alveolar epithelial type II cells. As a widely utilized model for lung adenocarcinoma, A-549 cells offer a robust platform for investigating epithelial-derived cytokine signaling, tumor?Cimmune interactions, and oncogenic processes in a lung-specific microenvironment.
Interleukin-27 (IL27) is a heterodimeric cytokine composed of EBI3 and IL27p28 subunits that binds to a receptor complex formed by IL27RA and gp130 (IL6ST). Ligand engagement activates associated Janus kinases JAK1 and JAK2, leading to phosphorylation of STAT1 and STAT3 transcription factors. Activated STAT1/STAT3 dimers translocate to the nucleus and regulate the expression of downstream targets such as TBX21, IL10, and SOCS1, thereby modulating T-helper cell differentiation and inflammatory responses. Upstream regulators of IL27 include interferon gamma (IFNG), Toll-like receptor (TLR) ligands, bacterial lipopolysaccharide (LPS), type I interferons, and interleukin-1 beta (IL1B).
Disruption of IL27 in A-549 cells allows dissection of the role of tumor-derived IL27 in the lung cancer microenvironment. Given that IL27 can exert both pro-inflammatory and anti-inflammatory effects depending on context, this knockout model is instrumental for evaluating how loss of epithelial IL27 alters immune cell recruitment, cytokine networks, and STAT-dependent signaling in lung adenocarcinoma. It enables the study of immune evasion mechanisms and the impact on cancer progression.
Researchers can employ these polyclonal knockout cells in a variety of experimental systems, including co-culture assays with immune effectors such as T cells or macrophages, cytokine secretion profiling by ELISA, and phospho-STAT analysis by flow cytometry or western blotting. Verification of knockout can be performed by RT-qPCR, western blotting, or DNA sequencing. Applications span lung cancer immunology, inflammatory signaling, and therapeutic target validation. For additional information and custom orders, please contact Ascent Research.
