Zinc oxide (ZnO) quantum dot (QD) is a promising inexpensive inorganic nanomaterials, of which potential toxic effects on biological systems and human health should be evaluated before biomedical application. In this study, the cytotoxicity of ZnO QDs was assessed using HeLa cervical cancer cell and HEK-293T human embryonic kidney cell lines. Cell viability was significantly decreased by treatment with 50 µg/ml ZnO QDs after only 6 h, and the cytotoxicity of ZnO QDs was higher in HEK-293T than in HeLa cells. ZnO QDs increased the level of reactive oxygen species and decreased the mitochondria membrane potential in a dose-dependent manner. Several gene expression involved in apoptosis was regulated by ZnO QDs, including bcl-2 gene and caspase. In HeLa cells, ZnO QDs significantly increased early and late apoptosis, but only late apoptosis was affected in HEK-293T cells. These findings will be helpful for future research and application of ZnO QDs in biomedicine.

BackgroundNumerous studies have shown that long noncoding RNA (lncRNA) is involved in gastric cancer (GC). A relevant microarray containing gastric cancer-related lncRNAs was downloaded from The Cancer Genome Atlas database.MethodsqRT-PCR was used to analyze LINC00565 and AKT3 expression in tumor tissues and cell lines. Proliferative, colony formation and apoptotic abilities of GC cells after transfection of sh-LINC00565 were determined by CCK-8, colony formation assay and flow cytometry, respectively. RIP was enrolled to detect the interaction between LINC00565, AKT3 and miR-665. Dual luciferase assay was used to confirm the relation between miR-665 and LINC00565 and AKT3.ResultsExpression level of LINC00565 in GC tissue was highly expressed in GC, which was negatively correlated to prognosis of GC patients. The results showed that knockdown of LINC00565 decreased proliferative and colony formation abilities, and induced apoptosis of GC cells. Pearson analysis showed that LINC00565 was positively correlated with AKT3. Besides, AKT3 was significantly up-regulated in GC. In addition, knockdown of LINC00565 down-regulated AKT3. In order to explore the mechanism, we found that miR-665 could bind to LINC00565 by bioinformatics. Dual-luciferase reporter gene assay and RIP assay both verified the binding relationship between miR-665 and AKT3. Finally, rescue experiments were carried out to explore whether AKT3 could reverse the anti-cancer effect of low-level LINC00565 on GC development.ConclusionIn summary, the expression of LINC00565 is upregulated in GC. LINC00565 can be used as the sponge of miR-665 to up-regulate the expression of AKT3, thus promoting the progression of GC.

Introduction: ZnO quantum dots (QDs) have drawn much attention recently as they are Cd-free, low-cost, and have excellent optical properties. With the expanded production and application of ZnO nanoparticles, concerns about their potential toxicity have also been raised. Materials and Methods: We used RNA sequencing (RNA-seq) to analyze the global gene expression of liver and lung tissues after ZnO QDs treatment. Differentially expressed genes (DEGs) were screened, with a fold change >1.5 and padj <0.05. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed, and padj <0.05 was considered significantly enriched. The RNA-seq results were validated by quantitative real-time polymerase chain reaction (qRT-PCR). Results: A total of 47 and 218 genes were significantly differentially expressed in the liver and lung. Eight GO terms were enriched in the liver and lung, and retinol metabolism and the peroxisome proliferator-activated receptor (PPAR) signaling pathway were shared in different tissues. Discussion: According to DEGs and pathway enrichment analyses, inflammation might be induced in liver and lung tissues after intravenous injection of ZnO QDs. These findings will be helpful for future research and application of ZnO QDs.