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The apoptosis of endothelial cells (ECs) induced by oxidized low-density lipoprotein (ox-LDL) is an important contributing factor in the pathogenesis of atherosclerosis. It has been reported that microRNA (miR)-106a-5p is overexpressed in atherosclerotic plaques and involved in angiogenesis. However, its role and underlying mechanisms in ox-LDL induced EC apoptosis remain to be fully understood. In the present study the expression of miR-106a-5p in human umbilical vein ECs (HUVECs) stimulated with ox-LDL was investigated using reverse transcription-quantitative PCR analysis. Cell viability and apoptosis were assessed by MTT assay and flow cytometry, respectively. Caspase-3 activity and reactive oxygen species (ROS) levels were determined by commercial kits. The interaction between miR-106a-5p and signal transducer and activator of transcription 3 (STAT3) mRNA was examined by luciferase reporter assay. It was found that ox-LDL treatment significantly increased the levels of miR-106a-5p in a dose-dependent manner in HUVECs. Moreover, these results demonstrated that ox-LDL treatment inhibited cell viability, promoted cell apoptosis, increased caspase-3 activity and ROS levels, whereas inhibition of miR-106a-5p reversed the effects of ox-LDL on HUVECs. In addition, it was shown that STAT3 is a direct target of miR-106a-5p in HUVECs, and silencing of STAT3 impaired the protective effects of miR-106a-5p inhibition on cell apoptosis and oxidative injury induced by ox-LDL. Collectively, these results indicated that miR-106a-5p participated in ox-LDL-stimulated apoptosis and oxidative injury in HUVECs by regulating STAT3. Thus, suggesting that miR-106a-5p/STAT3 may serve as a novel therapeutic target for atherosclerosis in the future. [ABSTRACT FROM AUTHOR]

The use of metal complexes containing phosphorus ligands as anticancer agents has not been well studied. In this work, eight novel half‐sandwich IrIII and RuII compounds with P^P‐chelating ligands have been synthesized and fully characterized, and alongside two crystal structures were reported. All eight complexes displayed highly potent antiproliferative activity, up to nine times more potent than the clinical anticancer drug cisplatin towards A549 lung cancer cells. Complex Ir1, which has a simpler structure and highly potent antiproliferative activity, was selected to investigate in further mechanistic studies. No hydrolysis and nucleobase binding occurred for complex Ir1. In order to elucidate subcellular localization, the self‐luminescence of the complex Ir1 was utilized. Ir1 can specifically target lysosomes and facilitate excessive production of reactive oxygen species, resulting in lysosomal membrane permeabilization in A549 cells. Release of cathepsin B and changes in the mitochondria membrane potential also contributed to the observed cytotoxicity of Ir1, which demonstrated an anticancer action mechanism that was different from that of cisplatin. The favorable results from biological and chemical research demonstrated that these types of complexes hold significant theranostic potential. The use of metal complexes containing phosphorus ligands as anticancer agents has not been well studied. In this work, eight novel half‐sandwich IrIII and RuII compounds with P^P‐chelating ligands have been synthesized and fully characterized. The favorable results of biological and chemical research demonstrated that these types of complexes hold significant theranostic potential. [ABSTRACT FROM AUTHOR]