The IL11 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the IL11 gene has been disrupted in the HGC-27 human gastric adenocarcinoma cell line. This product provides a heterogeneous pool of edited cells that serves as a robust loss-of-function model for interrogating IL11-dependent signaling pathways and tumor cell biology. The polyclonal format preserves genetic diversity, offering a representation of the editing outcomes across the cell population and minimizing biases associated with single-cell clonal selection.
HGC-27 is a widely utilized epithelial cell line originally derived from the metastatic lymph node of a patient with gastric adenocarcinoma. As a well-characterized model for gastric carcinoma, HGC-27 retains key features of gastric cancer biology, including constitutive activation of multiple growth factor and cytokine signaling pathways. This cell line is particularly suited for studying molecular mechanisms of gastric tumorigenesis, metastasis, and therapeutic resistance.
IL11 encodes a pleiotropic cytokine that signals through a heterodimeric receptor complex of IL11RA and gp130 (IL6ST). Ligand binding activates JAK1, JAK2, and TYK2, which phosphorylate STAT3. Activated STAT3 translocates to the nucleus and transcriptionally upregulates MYC, CCND1, and BCL2, driving cell cycle progression and survival. Parallel signaling via GRB2/SOS1/HRAS to MAPK/ERK (MAP2K1??MAPK3/1) and via PIK3CA to AKT1 amplifies proliferative and anti-apoptotic programs. SOCS3 and PTPN11 negatively regulate signaling. In gastric epithelial cells, IL11 expression is induced by upstream stimuli including TGFB1, IL1B, TNF, and NFKB1, and by Helicobacter pylori infection, linking inflammatory and fibrotic signals to oncogenic progression.
In the context of HGC-27 gastric cancer cells, constitutive IL11 signaling promotes a malignant phenotype characterized by enhanced proliferation, resistance to apoptosis, and increased invasive capacity. IL11 knockout in these cells disrupts the autocrine/paracrine loop that sustains JAK/STAT, MAPK/ERK, and PI3K/AKT pathway activation, thereby attenuating tumorigenic traits. This model is particularly valuable for dissecting IL11??s contribution to chemoresistance and for exploring its crosstalk with TGF-?? in driving epithelial-mesenchymal transition and metastasis. The polyclonal knockout pool avoids potential clonal artifacts, providing a more representative system for functional genomics and drug sensitivity studies.
This polyclonal IL11 knockout product supports a wide range of functional studies. Key assays include phospho-STAT3 immunoblotting, RT-qPCR for MYC and CCND1, MTT proliferation, Annexin V apoptosis, transwell migration, and cell cycle flow cytometry. Co-immunoprecipitation of IL11RA and gp130 and ELISA for secreted IL11 confirm pathway disruption. The cells are also suitable for in vivo xenograft tumor growth assays to evaluate metastasis and drug response. These tools support discovery of IL11 pathway inhibitors, investigation of tumor microenvironment crosstalk, and functional genomic screens. For further technical details or to discuss custom solutions, please contact Ascent Research.
