ABSTRACT
Circular RNAs (circRNAs) have been shown to play a functional role in a variety of cancers. However, few studies on circRNAs in estrogen receptor-positive breast cancer have been conducted. Here, we investigated the role of circRNA circTP63 in estrogen receptor-positive breast cancer progression and malignant behaviors. First, we observed increased expression of circTP63 in MCF7 cells relative to normal human mammary epithelial cell lines, such as DU4475 and MCF-10A, and the changed oncogenicity of MCF7 cells correlated with circTP63 overexpression and downregulation. Interestingly, a series of gain- and loss-of-function assays revealed that a higher level of FOXM1 was closely associated with MCF7 malignant behaviors induced by circTP63 overexpression. Further investigations showed that circTP63 sponged to miR-873-3p, which targeted FOXM1 mRNA and inhibited its expression. Mechanistically, circTP63 binds to miR-873-3p and prevents the targeting of FOXM1, thus inducing the progression and malignant behaviors of estrogen receptor-positive breast cancer, such as cell proliferation, cell cycle dysregulation, invasion, migration and even tumor growth. CircTP63 might be a potential biomarker or target to treat estrogen receptor-positive breast cancer patients in the future.
Subject(s)
Breast Neoplasms/pathology , Forkhead Box Protein M1/metabolism , Gene Expression Regulation, Neoplastic , MicroRNAs/genetics , RNA, Circular/genetics , Receptors, Estrogen/metabolism , Transcription Factors/genetics , Tumor Suppressor Proteins/genetics , Animals , Apoptosis , Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Breast Neoplasms/genetics , Breast Neoplasms/metabolism , Cell Cycle , Cell Proliferation , Epithelial-Mesenchymal Transition , Female , Forkhead Box Protein M1/genetics , Humans , Mice , Mice, Inbred BALB C , Mice, Nude , Neoplasm Invasiveness , Tumor Cells, Cultured , Xenograft Model Antitumor AssaysABSTRACT
First-principles calculations were used to investigate the electronic properties of the SiC/GeC nanosheet (the thickness was about 8 Å). With no electric field (E-field), the SiC/GeC nanosheet was shown to have a direct bandgap of 1.90 eV. In the band structure, the valence band of the SiC/GeC nanosheet was mainly made up of C-p, while the conduction band was mainly made up of C-p, Si-p, and Ge-p, respectively. Application of the E-field to the SiC/GeC nanosheet was found to facilitate modulation of the bandgap, regularly reducing it to zero, which was linked to the direction and strength of the E-field. The major bandgap modulation was attributed to the migration of C-p, Si-p, and Ge-p orbitals around the Fermi level. Our conclusions might give some theoretical guidance for the development and application of the SiC/GeC nanosheet.
ABSTRACT
OBJECTIVE: This work aimed to identify the risk factors of Helicobacter pylori (H. pylori) infection in preschool children and provide effective measures for the prevention and reduction of the incidence of H. pylori infections. METHODS: A total of 204 children from two kindergartens in Suzhou city were recruited through a questionnaire survey. Risk factors were selected through the single factor paired data χ² test and multiple factor Logistic regression analysis. Oral and gastric H. pylori infections were detected by using H. pylori saliva detection (HPS) and ¹³C-urea breath test (¹³C-UBT). Special toothpaste for H. pylori control was selected for oral cleaning. Oral H. pylori infection rates at 2 months after special toothpaste treatment were examined by using HPS. RESULTS: The high-risk factors of H. pylori infections among preschool children included poor personal hygiene habits, such as the nibbling of fingers and the avoidance of hand-washing before meals, diet, and parent's history of stomach disease. Among the 204 subjects enrolled in this study, 158 (77.45%), 37 (18.14%), and 28 (13.73%) were HPS positive, ¹³C-UBT positive, and HPS and ¹³C-UBT positive, respectively. The incidence of oral H. pylori infections was significantly higher than that of gastric H. pylori infections (P<0.01). The positive rate of infections significantly decreased after special toothpaste treatment (P<0.01). This result indicates that the intervention was effective. CONCLUSIONS: Children must receive education on good eating habits. Individualized dining habits or the use of public chopsticks must be implemented. H. pylori infections must be detected as early as possible. Specific toothpaste for oral cleaning must be selected. These approaches could drastically prevent or reduce the incidence of H. pylori infections among preschool children.
Subject(s)
Helicobacter Infections , Helicobacter pylori , Breath Tests , Child, Preschool , Helicobacter Infections/epidemiology , Humans , Risk Factors , UreaABSTRACT
Hyperuricemia and artery atherosclerosis are closely associated and, as a classic inflammatory biomarker, tumor necrosis factorα (TNFα) has a direct role in atherogenesis. In the present study, it was demonstrated that uric acid was capable of inducing the generation of TNFα in vascular smooth muscle cells (VSMCs). The expression levels of proteins were detected using enzymelinked immunosorbent assays and western blot analysis. The expression levels of mRNAs were determined using reverse transcriptionquantitative polymerase chain reaction analysis, and superoxide anion levels were detected using a fluorescence microscope. From the results, it was concluded that uric acid induced the expression of TNFα in the VSMCs. The antioxidant, Nacetylcysteine, eliminated the uric acidinduced expression of TNFα. In addition, uric acid increased the level of reactive oxygen species (ROS) and activated the phosphorylation of p38. Subsequent experiments confirmed that the p38 mitogenactivated protein kinase (MAPK) inhibitor, SB203580, and nuclear factor (NF)κB inhibitor, pyrrolidine dithiocarbamate, eliminated the uric acidinduced expression of TNFα. It was demonstrated that uric acid induced the expression of TNFα via the ROSMAPKNFκB signaling pathway in VSMCs, providing novel evidence supporting the proinflammatory and proatherosclerotic effects of uric acid.