Abstract
Objective: The destruction of vascular endothelial function is an important mechanism for the formation of aortic dissection. Here, we aim to investigate the role of lncRNA Ftx in the biological functions of vascular endothelial cells, as well as the key proteins it regulates, to further explore the potential regulatory role of Ftx on the function of vascular endothelial cells in the pathogenesis of aortic dissection.Experimental Design: The expression of lncRNA Ftx was measured in aortic dissection tissues（n＝12）and age- and sex-matched patients with hypertension tissues（n＝12）. Loss and Gain-of-Function cell Models was constructed using the lentivirus mediated Ftx/Sh-Ftx transfection in HUVECs. The quantitative proteomics was performed to profile the differentially expressed proteins in cell models and further defined the crucial molecules and pathways involved in the carcinogenesis process of lncRNA Ftx. Cell experiments was conducted for valuable proteins to verify the regulatory effect by Ftx.Results: The results of clinical specimen examination showed that LncRNA Ftx was significantly over-expressed in aortic dissection tissue compared with normal aortic tissue. A total of 4348 proteins were quantified by protein mass spectrometry, which are involved in various biological processes and related signaling pathways including cell proliferation, cell apoptosis, cell functional changes and cell metabolism. Interestingly,CBX1, is a protein associated with proliferation and apoptosis of vascular endothelial cells,was up-regulated in the absence of LncRNA Ftx and down-regulated in the overexpression of LncRNA Ftx, which was further verified in HUVECs. Conclusion: This study showed that the intervention of LncRNA Ftx expression in vascular endothelial cells can regulate multiple biological processes such as cell proliferation and apoptosis, thus affecting the progression of aortic dissection. In this process, LncRNA Ftx may have a negative regulation effect on CBX1. which provided a new perspective for the mechanism of gastric cancer progression, and thus identified potential therapeutic targets for gastric cancer.
Cimetidine inhibits the adhesion of gastric cancer cells expressing high levels of sialyl Lewis x in human vascular endothelial cells by blocking E-selectin expression
