The IL11 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma line, engineered to disrupt the interleukin-11 (IL11) gene. This loss-of-function model eliminates endogenous IL-11 expression, providing researchers with a robust tool to dissect IL-11-dependent signaling in ovarian cancer biology. The polyclonal format represents a heterogeneous pool of edited cells, reflecting a range of null alleles without clonal selection, thereby preserving population-level responses and minimizing clone-specific artifacts in downstream assays.
The A2780 cell line was originally isolated from an untreated patient with epithelial ovarian carcinoma and is well-characterized as a cisplatin-sensitive model. It is widely utilized to investigate tumor cell proliferation, invasion, chemoresistance mechanisms, and the epithelial-mesenchymal transition (EMT). A2780 cells retain key features of high-grade serous ovarian cancer, including proficient DNA repair pathways and responsiveness to inflammatory and fibrotic stimuli, making them an appropriate host for studying IL-11??s pleiotropic effects in a disease-relevant context.
Interleukin-11 is a secreted cytokine of the IL-6 family that signals via a receptor complex composed of IL11RA and the gp130 co-receptor (IL6ST). Ligand binding triggers phosphorylation of associated Janus kinases (JAK1, JAK2, TYK2) and subsequent activation of STAT3, ERK1/2, and AKT pathways. Upstream, IL-11 transcription is induced by factors such as TGFB1, IL1B, and TNF, often through STAT3- and NF-??B-dependent mechanisms. Downstream, IL-11 promotes expression of pro-survival (BCL2L1, CCND1), pro-invasive (MMP2, MMP9, VEGF), and pro-fibrotic (ACTA2, COL1A1, FN1, CTGF, SERPINE1) target genes, while also reinforcing TGFB1 signaling and EMT regulators including SNAI1 and TWIST1. In the tumor microenvironment, IL-11 participates in autocrine and paracrine loops that sustain cancer-associated fibroblast activation and matrix remodeling.
In A2780 cells, CRISPR-mediated knockout of IL-11 ablates the major axis of IL-11/IL11RA/gp130 signaling, markedly attenuating STAT3, ERK, and AKT phosphorylation. This disruption impairs ovarian cancer cell proliferation, migration, and invasion, while also dampening pro-fibrotic gene expression and EMT. Consequently, the knockout model is particularly valuable for examining how IL-11 contributes to cisplatin resistance and evaluating whether loss of IL-11 sensitizes cells to standard-of-care chemotherapy. Additionally, the cells allow dissection of cross-talk between IL-11 and TGF-?? pathways, as IL-11 is both induced by and can amplify TGF-?? responses.
Typical research applications include functional analyses of IL-11 in ovarian cancer growth using MTT or CCK-8 assays, Transwell migration and invasion studies, and wound healing experiments. The cells are suitable for chemosensitivity testing with cisplatin or paclitaxel, apoptosis measurement by Annexin V flow cytometry, and ELISAs to confirm loss of secreted IL-11 protein. Transcriptome profiling via RNA-seq can uncover global gene expression changes upon IL-11 loss, while co-culture with cancer-associated fibroblasts permits investigation of paracrine fibrotic signaling. In vivo, these cells can be employed in xenograft models to assess tumor progression and therapeutic response. For further information, please contact Ascent Research.
