Extracellular vesicles (EVs) are mediators of communication between cancer cells and the surrounding tumor microenvironment. EV content is able to influence key tumorigenic changes including invasion, metastasis, and inducing pro-tumor changes in the stroma. MiR-142-3p is a known tumor suppressor in LAC and was recently shown to be enriched within LAC EVs, indicating its potential as a key signaling miRNA. Our research demonstrates the role EV associated miR-142-3p plays when transferred from LAC cells to both endothelial and fibroblast cells. We demonstrate that transfer of miR-142-3p in LAC EVs to endothelial cells promotes angiogenesis through inhibition of TGFβR1. Additionally, we show EV associated miR-142-3p promotes the cancer-associated fibroblast phenotype in lung fibroblast cells which we show is independent of TGFβ signaling. These findings suggest that miR-142-3p within LAC EVs can be transferred from LAC cells to both endothelial and fibroblast cells to promote tumor associated changes.
Keywords: MiRNA; NSCLC; exosomes; extracellular vesicles; lung adenocarcinoma.
© 2018 Wiley Periodicals, Inc.