Despite intensive research activities, there are still many major knowledge gaps over the potential adverse effects of titanium dioxide nanoparticles (TiO2‐NPs), one of the most widely produced and used nanoparticles, on human cardiovascular health and the underlying mechanisms. In the present study, alkaline comet assay and cytokinesis‐block micronucleus test were employed to determine the genotoxic potentials of four sizes (100, 50, 30, and 10 nm) of anatase TiO2‐NPs to human umbilical vein endothelial cells (HUVECs) in culture. Also, the intracellular redox statuses were explored through the measurement of the levels of reactive oxygen species (ROS) and reduced glutathione (GSH) with kits, respectively. Meanwhile, the protein levels of nuclear factor erythroid 2‐related factor 2 (Nrf2) were also detected by western blot. The results showed that at the exposed levels (1, 5, and 25 μg/mL), all the four sizes of TiO2‐NPs could elicit an increase of both DNA damage and MN frequency in HUVECs in culture, with a positive dose‐dependent and negative size‐dependent effect relationship (T100 < T50 < T30 < T10). Also, increased levels of intracellular ROS, but decreased levels of GSH, were found in all the TiO2‐NP‐treated groups. Intriguingly, a very similar manner of dose‐dependent and size‐dependent effect relationship was observed between the ROS test and both comet assay and MN test, but contrary to that of GSH assay. Correspondingly, the levels of Nrf2 protein were also elevated in the TiO2‐NP‐exposed HUVECs, with an inversely size‐dependent effect relationship. These findings indicated that induction of oxidative stress and subsequent genotoxicity might be an important biological mechanism by which TiO2‐NP exposure would cause detrimental effects to human cardiovascular health.
Deregulation of microRNA (miR)-193b has been revealed to be associated with the proliferation of liver cells. However, the interaction between miR-193b and their targets inducing liver cancer remains largely unknown. The aim of the present study was to investigate the hypothesis that miR-193b affects the proliferation of liver cancer cells. In the present study, the overall survival of patients with liver cancer and low fold change of miR-193b was higher compared with that of patients with liver cancer patients and high fold change of miR-193b. The expression level of myeloid cell leukemia-1 (Mcl-1) in patients with liver cancer was lower compared with in the control group. The results of the present study demonstrated that downregulation of miR-193b suppressed the proliferation and induced apoptosis of liver cancer cells, and inhibited the Mcl-1 protein expression level in liver cancer cells. Upregulation of miR-193b increased cell proliferation and decreased apoptosis of liver cancer cells and promoted the expression level of Mcl-1 protein. The results of the present study demonstrated that the expression of miR-193b as a novel tumor suppressor serves an important role in the proliferation of liver cancer cells by mediating Mcl-1 expression.
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