Skip to main content
Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: Single-cell deconvolution algorithms analysis unveils autocrine IL11-mediated resistance to docetaxel in prostate cancer via activation of the JAK1/STAT4 pathway

Fig. 7

Analysis of IL-11-mediated signalling in prostate cancer cell lines. A Random forest analysis indicating the error rate as a function of the number of trees, with key genes labelled for their variable importance in the model. B Gene set enrichment analysis (GSEA) showing the running enrichment scores for selected hallmark gene sets across a ranked list of genes from the dataset. The JAK/STAT signalling pathway is emphasized, indicating its involvement in the response to IL-11. C Network representation of the protein‒protein interaction (PPI) focused on IL-11, with edge colours representing the type of interaction and node size correlating with the number of interactions per protein. D Bar graph illustrating the fold change in expression levels of JAK family kinases (JAK1, JAK2, JAK3, TYK3) upon alterations in IL-11 in prostate cancer cell lines. E Bar graph representing the fold change in expression levels of STAT family proteins (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B, STAT6) upon alteration of IL-11 in the same cell lines. F Western blot analysis showing protein expression of IL-11 and IL-11RA and the phosphorylation status of JAK1 and STAT4 in response to IL-11 treatment across different prostate cancer cell lines (PC3, DU145, LNCAP, 22RV1). G: Western blot analysis comparing protein expression and phosphorylation of JAK1 and STAT4 upon neutralization of IL-11 or IL-11 antagonist in PC3 and DU145 cell lines

Back to article page