精品文档---下载后可任意编辑MicroRNA--126 在三氧化二砷抑制人脐静脉内皮细胞中的作用机制的开题报告Title: Mechanism of MicroRNA-126 Suppression in Arsenic Trioxide Inhibited Human Umbilical Vein Endothelial CellsBackground:Arsenic trioxide (ATO) is a chemotherapeutic agent that has been used for the treatment of various types of cancers, including acute promyelocytic leukemia and solid tumors. However, the use of ATO is associated with several side effects, including cardiovascular toxicity. It has been shown that ATO can inhibit the proliferation and migration of human umbilical vein endothelial cells (HUVECs), which are important in maintaining vascular homeostasis. MicroRNA-126 (miR-126) has been implicated in regulating the function of endothelial cells and is downregulated in various pathologies, such as atherosclerosis and cancer. The role of miR-126 in ATO-treated HUVECs remains unclear.Objective:Our objective is to investigate the mechanism by which miR-126 is suppressed in ATO-treated HUVECs.Methods:We will treat HUVECs with different concentrations of ATO and evaluate the expression of miR-126 using qRT-PCR. Western blotting will be performed to assess the levels of proteins involved in the miR-126 pathway, such as vascular endothelial growth factor-A (VEGF-A) and p85α regulatory subunit of phosphatidylinositol 3-kinase (PI3K). The binding of miR-126 to its target genes will be determined using luciferase reporter assays. Cell proliferation and migration assays will also be performed to evaluate the effects of miR-126 suppression on the function of HUVECs.Expected results:We expect to observe a downregulation of miR-126 in ATO-treated HUVECs, which may be due to the inhibition of VEGF-A and PI3K expression. We also expect to demonstrate that miR-126 can regulate the proliferation and migration of 精品文档---下载后可任意编辑HUVECs, and that the suppression of miR-126 may contribute to the anti-proliferative and anti-migratory effects of ATO on HUVECs.Significance:This study will provide insights into the mechanism by which ATO affects the function of endothelial cells and may identify miR-126 as a potential therapeutic target for reducing the cardiovascular toxicity of ATO treatment.
