ABSTRACT
Objective To investigate the effects of lncRNA FENDRR on the proliferation, migration, invasion and apoptosis of LUSC H226 cells and its molecular mechanism. Methods The expression levels of FENDRR in normal lung epithelial cells BEAS, lung adenocarcinoma A549 and H1299 cells and LUSC H226 cells were detected by qRT-PCR. H226 cells were transfected with FENDRR-siRNA as the experimental group, or with FENDRR-siNC as a negative control group. Cell proliferation was detected by CCK-8 assay. Cell migration and invasion were detected by Transwell assay. Cell apoptosis was detected by flow cytometry. The protein expression levels of MEK, p-MEK, ERK and p-ERK were determined by Western blot. Results FENDRR levels in H226 cells were significantly lower than those in normal lung epithelial cells. Compared with the negative control group, the knockdown of FENDRR could significantly promote the proliferation, migration and invasion of H226 cells, inhibit the cell apoptosis, and increase the protein levels of p-MEK and p-ERK. The addition of ERK inhibitor U0126 rescued the effect of FENDRR knockdown on H226 cells. Conclusions The knockdown of lncRNA FENDRR can promote the proliferation, migration and inhibit the apoptosis of H226 cells through ERK/MAPK pathway.
ABSTRACT
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is an inflammatory lung injury induced by a variety of factors, and these diseases are associated with high rates of mortality due to the lack of effective treatments. Based on the latest research in ALI/ARDS, it is widely accepted that generalized inflammatory responses play a critical role in initiating and developing process of ALI/ARDS. We make a brief review on the immune-pathogenesis and the signaling pathways of ALI/ARDS from the perspective of inflammation, thereby helping develop novel therapeutic strategy for treatment of patients with ALI/ARDS.