Panoply™ Human IL11 Over-expressing Stable Cell Line

Cytokines play a pivotal role in tumorigenesis and serve as potential targets for cancer therapy. While interleukin-6 (IL-6) has garnered significant attention, interleukin-11 (IL-11)-another member of the IL-6 family-has long been overlooked, and little is known about its specific function in non-small cell lung cancer (NSCLC). In this study, researchers investigated the role of IL-11 in NSCLC and its underlying mechanisms. The results demonstrated that IL-11 was highly expressed in NSCLC samples compared to normal tissues and was associated with poor patient prognosis. In vitro and in vivo experiments indicated that IL-11 promotes cell proliferation and tumorigenesis. Furthermore, IL-11 enhanced cell migration and invasion capabilities and induced epithelial-mesenchymal transition (EMT). Experimental models revealed that IL-11 activated the AKT and STAT3 signaling pathways. Additionally, the researchers found that hypoxic conditions induced IL-11 expression in NSCLC cells; the upregulation of hypoxia-inducible factor 1-alpha (HIF1α)-induced by deferoxamine (DFX) or dimethyloxalylglycine (DMOG)-also promoted IL-11 expression in these cells. These findings suggest that IL-11 functions as an oncogene in NSCLC, and elucidating its mechanism of action may offer new insights for NSCLC therapy.

To further investigate the significance of IL-11 in non-small cell lung cancer (NSCLC), researchers examined the role of IL-11 in cell invasion and metastasis. Transwell migration assay results showed that IL-11 knockdown inhibited the migration of A549 and H1299 cells (Figure 1A and B). Conversely, migratory capacity was enhanced in IL-11- overexpressing A549 and H1299 cells (Figure 1E and F). Next, the researchers validated these findings using a wound healing assay; IL-11 inhibition significantly attenuated the migratory ability of A549 cells (Figure 1D). They also assessed invasive capacity using Matrigel-coated Boyden chambers. As shown in Figure 1A and 1C, the invasive capacity of both A549 and H1299 cell lines decreased following IL-11 inhibition. In contrast, enhanced invasion was observed in IL-11- overexpressing cells (Figure 1E and 1G). Treatment with an IL-11 neutralizing antibody reversed the IL-11-induced enhancement of invasion and migration (Figure 1E–1G).

Figure 1. IL-11 promotes NSCLC cell invasion and migration in vitro and lung colony formation in vivo. (Zhao M, et al., 2018)