Exosomes-mediated transfer LINC00691 regulates the formation of CAFs and promotes the progression of gastric cancer

Abstract Objective To find the expression pattern of serum exosomal LINC00691 in GC patients and the correlation between the level of serum exosomal LINC00691 and the pathology and prognosis of gastric cancer patients. Methods We treated normal fibroblasts (NFs) with LINC00691-rich GC cell culture supernatant or exosomes and detected the activation markers and biological functions of the fibroblasts. Results It was found that the level of LINC00691 was significantly increased, the cell proliferation and migration were noticeably enhanced, and the ability to accelerate GC cell proliferation and invasion was promoted after treated with GC exosomes, which means that the induced fibroblasts gained the properties of cancer-associated fibroblasts (CAFs). In addition, we found that knockdown of LINC00691 and the use of the JAK2/STAT3 signaling pathway inhibitor ruxolitinib effectively deprived the effects of exosome-containing GC cell supernatants on NFs. Conclusion Our study suggested that exosomal LINC00691 promoted the transformation from NFs to CAFs depending on JAK2/STAT3 signaling pathway as a potential diagnostic biomarker for GC.