Interaction between non-small-cell lung cancer cells and fibroblasts via enhancement of TGF-β signaling by IL-6

Regulation of Gene Expression by Sodium Valproate in Epithelial-to-Mesenchymal Transition

“…TGF-b1-induced EMT model using A549 cell line is usually used as lung cancer model [21][22][23][24] or pulmonary fibrosis model [8,25,26]. Our study demonstrated that TGF-b1 caused a decrease of histone acetylation, and is the first to report that the acetylation of histone H3K27 is drastically down-regulated compared with that of other histone acetylation residues during TGF-b1-induced EMT model in A549 whole cells, while the methylation status of histone H3K27 remained unchanged.…”

IL-6 Secreted from Cancer-Associated Fibroblasts Mediates Chemoresistance in NSCLC by Increasing Epithelial-Mesenchymal Transition Signaling

“…15 Furthermore, crosstalk between IL-6 and TGF-β is associated with malignant features including EMT in several cancers. 10,16,17 The purpose of this study was to clarify the role of the TGF-β−IL-6 axis in communication between CAFs and NSCLC cells for chemo-or chemoradio-resistance using a NSCLC cell lines as well as clinical samples.…”

Chronic Inflammation and Cytokines in the Tumor Microenvironment

“…Extensive evidence supports the notion that EMT can be induced by proinflammatory cytokines. TNF- α and IL-6 may synergistically nudge the TGF- β signaling pathway towards EMT progression (Figures 1(b) and 1(c)) [21, 145]. Both cytokines promote NF- κ B activation, which regulates the expression of transcription factors involved in EMT, orchestrating the effects of Snail1, Snail2, Twist, ZEB1, and ZEB2 [146, 147].…”