Fig 2: Inhibition of IL-17 signaling mediated the effects of downregulation on OS cell migration and invasion. (A) Western blot showed that downstream targets of IL-17 signaling (CEBPB, MMP1, MMP3, and MMP9) decreased activation in the cells relative to control. (B) qPCR showed a significant decrease in RNA levels. (C) ELISA analysis showed IL-17A levels decreased after KRAS knockdown. (D) Representative images showed markers of IL-17 signaling in high or low expression of KRAS in OS tissues. (E) Western blot assay and qPCR showed the level of IL-17A was sharply increased in OS cells transfected with lentivirus(Lv-IL-17A). (F) Upregulation of IL-17A increased the migration of OS cells in wound-healing assays. (G) The overexpression of IL-17A markedly enhanced the migration (up) and invasion (down) capabilities of OS cells, as assessed by transwell analysis. The data are presented as mean ± SD (n = 3). **p < .01 or ***p < .001 signifies a statistically significant difference between the specified groups.

Fig 3: CEBPB upregulates ERK1/2 activity and affects the malignant progression of OC through SOS1 in vivo. A Tumor volume of transplanted tumors in nude mice; B body weight of nude mice; C pathological changes of nude mice were observed by HE staining, and Ki67 expression was detected by IHC staining (scale bar = 10 μm); D statistical diagram of IHC results; E, F The expression of CEBPB was detected by immunofluorescence and its statistical diagram (scale bar = 10 μm); G, H The expression of SOS1 was detected by immunofluorescence and its statistical graph (scale bar = 10 μm); I, J The apoptosis of tumor tissue was detected by TUNEL staining and its statistics graph (scale bar = 10 μm); K, L the levels of CEBPB, SOS1, and phosphorylated ERK1/2 were detected by western blotting and their statistical graphs. Plots are representative of three independent replicate experiments ( n = 3 per group per experiment). *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not statistically significant

Fig 4: The regulatory effect of changes in CEBPB expression on the MAPK signaling pathway. A Heatmap of genes in the MAPK pathway in SKOV3 cells; B Heatmap of genes in the MAPK pathway in A2780 cells; C: The expression of MAP4K1, PAK2, MKNK1 and SOS1 in SKOV3 and A2780 cells was detected by Western blotting and their statistical graphs. Plots are representative of three independent replicate experiments ( n = 3 per group per experiment). *, p < 0.05; ***, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not statistically significant

Fig 5: CEBPB promotes malignant behavior of OC cells. A, B the overexpression and knockdown efficiency of CEBPB was detected by qRT-PCR (# represents p < 0.05 in the comparison with the NC group); C the proliferation ability of SKOV3 and A2780 cells was detected by CCK-8 kit (# represents p < 0.05 in the comparison with the NC group); D the colony formation ability of cells was detected by colony formation assay and its statistical graph (scale bar = 50 μm); E cell invasion ability was detected by Transwell assay and its statistical graph (scale bar = 50 μm); F cell migration ability was detected by scratch healing assay and its statistical graph (scale bar = 50 μm); G, H cell apoptosis rate was detected by flow cytometry and its statistical graph; I, J cell cycle changes were assessed by flow cytometry and its statistical graph. Plots are representative of three independent replicate experiments ( n = 3 per group per experiment). *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not statistically significant