Interplay between YB-1 and IL-6 promotes the metastatic phenotype in breast cancer cells

摘要: Epithelial to mesenchymal transition (EMT) induces cell plasticity and promotes metastasis. The multifunctional oncoprotein Y-box binding protein-1 (YB-1) the pleiotropic cytokine interleukin 6 (IL-6) have both been implicated in tumor metastasis EMT, but via distinct pathways. Here, we show that direct interplay between YB-1 IL-6 regulates breast cancer Overexpression of lines induced production while stimulation with increased expression phosphorylation. Either approach was sufficient induce EMT features, including migration invasion. Silencing partially reverted blocked effect inhibition signaling phenotype by overexpression, demonstrating a clear YB-1/IL-6 interdependence. Our findings describe novel network which IL-6, vice versa, creating positive feed-forward loop driving EMT-like metastatic features during progression. Identification partners or pathways underlying this co-dependence may uncover therapeutic opportunities.