Chronic stress resulted in poor prognosis of cancer patients in the clinic. This study aimed to explore the mechanism by which chronic stress promotes the progression of lung adenocarcinoma (LUAD) through circRPPH1/miR-326 axis. Chronic stress-induced LUAD in vitro and in vivo models were established in A549 cells and C57BL/6 male mice. Sucrose preference test (SPT) and forced-swimming test (FST) were used for in vivo model evaluation. qRT-PCR and western blot were used to detect mRNA and protein levels. Cell proliferation, migration and invasion were also evaluated. Luciferase reporter assay was for target gene verification. In A549 cells, acetylcholine (ACh) -induced chronic stress contributed to the upregulation of circRPPH1. circRPPH1 knockdown remitted the carcinogenic effect of chronic stress on A549 cells. circRPPH1 serves as a sponger of miR-326, and miR-326 downregulation neutralized the beneficial role against tumor cell function and EMT in vitro. In vivo, circRPPH1 knockdown reduced the tumor volume and EMT-related protein levels of tumor-bearing mice under chronic stress treatment, while miR-326 antagomir co-transfection neutralized the effect. LARP1 might be the target gene of circRPPH1/miR-326 axis in CUMS mice. circRPPH1/miR-326 axis was involved in chronic stress-promoted progression and metastasis of LUAD.
Xiang et al. (Fri,) studied this question.