2020
DOI: 10.1158/1541-7786.mcr-19-1181 View full text |Buy / Rent full text
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Abstract: Although frequently associated with tumor progression, inflammatory cytokines initially restrain transformation by inducing senescence, a key tumor-suppressive barrier. Here, we demonstrate that the inflammatory cytokine, oncostatin M, activates a mesenchymal/stem cell (SC) program that engages cytokine-induced senescence (CIS) in normal human epithelial cells. CIS is driven by Snail induction and requires cooperation between STAT3 and the TGFβ effector, SMAD3. Importantly, as cells escape CIS, they retain the… Show more

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“…Recently, knockdown of OSMR expression in gastric cancer cells was shown to significantly inhibit cell proliferation, migration, invasion and EMP in vitro, as well as tumorigenesis and metastasis in vivo induced by OSM/STAT3/focal adhesion kinase (FAK)/proto-oncogene tyrosine-protein kinase Src (Src) signalling [ 47 ]. However, OSM-induced stemness and the CSC-like phenotype have been both attributed not only to STAT3 but also to PI3K kinase activation [ 48 , 49 , 50 ]. In non-transformed prostate cells, OSM, but not IL-6, was shown to induce EMP markers, increase migration in 2D and promote the pro-invasive dissemination of cells out of 3D spheroids.…”
Section: Role Of Il-6 and Osm In Epithelial–mesenchymal Plasticitymentioning
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“…Recently, knockdown of OSMR expression in gastric cancer cells was shown to significantly inhibit cell proliferation, migration, invasion and EMP in vitro, as well as tumorigenesis and metastasis in vivo induced by OSM/STAT3/focal adhesion kinase (FAK)/proto-oncogene tyrosine-protein kinase Src (Src) signalling [ 47 ]. However, OSM-induced stemness and the CSC-like phenotype have been both attributed not only to STAT3 but also to PI3K kinase activation [ 48 , 49 , 50 ]. In non-transformed prostate cells, OSM, but not IL-6, was shown to induce EMP markers, increase migration in 2D and promote the pro-invasive dissemination of cells out of 3D spheroids.…”
Section: Role Of Il-6 and Osm In Epithelial–mesenchymal Plasticitymentioning
“…Therefore, a plethora of complex interactions exist between the IL-6 cytokine family and other classical pathways inducing EMP and stemness, such as the epidermal growth factor receptor (EGFR) [ 52 , 53 ], insulin-like growth factor receptor 1 (IGF1R) [ 54 , 55 , 56 ], IL-8 [ 57 ], Wnt/β-catenin [ 58 ] or transforming growth factor-β (TGF-β)/SMAD pathways. Cooperative STAT3/SMAD complexes have been shown to be required for IL-6-, OSM- and TGF-β-induced EMP, invasiveness and stemness in breast, lung and biliary cancers, with a strong synergy between both the JAK/STAT3 and TGF-β /SMAD pathways [ 43 , 49 , 50 , 59 , 60 ]. Moreover, a recent study demonstrated that IFN-β impairs EMP by interfering with the STAT3/SMAD3/Snail axis that links OSM and TGF-β signalling [ 61 ].…”
Section: Role Of Il-6 and Osm In Epithelial–mesenchymal Plasticitymentioning
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“…Palbociclib in combination with letrozole significantly prolonged median progression-free survival (PFS) compared with placebo plus letrozole (27.6 vs 14.5 months) (Rugo et al, 2019). Although the effects of palbociclib in TNBC are not well-documented, cell cycle inhibition by palbociclib in MDA-MB-231 suggests its potential use to treat TNBC tumors Huang, Wu and Li, 2020;Bryson et al, 2021;Jost et al, 2021). In addition, beneficial effects have already been found in TNBC by combining palbociclib plus other apoptotic drugs in vitro and in vivo.…”
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