Knockdown of lncRNA H19 inhibits abnormal differentiation of small intestinal epithelial cells in diabetic mice.

Diabetes mellitus (DM) comprises a group of metabolic diseases characterized by insulin deficiency or resistance and hyperglycemia. We previously reported the presence of abnormal differentiation of small intestinal epithelial cells (IECs) in diabetic mice, but the exact mechanism of this phenomenon has not been thoroughly elucidated to date. In this study, we found that H19 was markedly upregulated in IECs of DM mice. H19 knockdown significantly inhibited abnormal differentiation of IECs in DM mice. Bioinformatics analysis identified miR-141-3p as a candidate for H19. Based on luciferase reporter assays, we found that miR-141-3p directly targeted H19. Luciferase reporter assays also showed that miR-141-3p could directly target ß-catenin. Furthermore, H19 might act as an endogenous "sponge" by competing for miR-141-3p binding to regulate miRNA targets in vitro and in vivo. In summary, our findings provide the first evidence supporting the role of H19 in IECs of DM mice, and miR-141-3p targets not only protein-coding genes but also the lncRNA H19.

A non-polluting method for rapidly purifying uranium-containing wastewater and efficiently recovering uranium through electrochemical mineralization and oxidative roasting.

Iron-based materials have been widely used for treating uranium-containing wastewater. However, the iron-uranium solids originating by treating radioactive water through pollutant transfer methods has become a new uncontrolled source of persistent radioactive pollution. The safe disposal of such hazardous waste is not yet well-resolved. The electrochemical mineralization method was developed to rapidly purify uranium-containing wastewater through lattice doping in magnetite and recover uranium without generating any pollutants. An unexpected isolation of U3O8 from uranium-doped magnetite was discovered through in-situ XRD with a temperature variation from 300 °C to 700 °C. Through HRTEM and DFT calculation, it was confirmed that the destruction of the inverse spinel crystal structure during the gradual transformation of magnetite into γ-Fe2O3 and α-Fe2O3 promoted the migration, aggregation, and isolation of uranium atoms. Uniquely generated U3O8 and Fe2O3 were easily separated and over 80% uranium and 99.5% iron could be recovered. These results demonstrate a new strategy for uranium utilization and the environmentally friendly treatment of uranium-containing wastewater.

The lncRNA ZEB1-AS1 sponges miR-181a-5p to promote colorectal cancer cell proliferation by regulating Wnt/ß-catenin signaling.

Long noncoding RNAs (lncRNAs) are important regulators of the biological functions and underlying molecular mechanisms of colorectal cancer (CRC). However, the role of the lncRNA ZEB1-AS1 in CRC is not thoroughly understood. In this study, we found that ZEB1-AS1 was markedly upregulated in CRC. ZEB1-AS1 knockdown significantly suppressed CRC cell proliferation and induced apoptosis, whereas enhanced expression of ZEB1-AS1 had the opposite effect. Bioinformatics analysis identified miR-181a-5p as a candidate target of ZEB1-AS1. Moreover, we found an inverse correlation between ZEB1-AS1 and miR-181a-5p expression in CRC tissue. Inhibition of miR-181a-5p significantly upregulated ZEB1-AS1, whereas overexpression of miR-181a-5p had the opposite effect, suggesting that ZEB1-AS1 is negatively regulated by miR-181a-5p. Using luciferase reporter and RIP assays, we found that miR-181a-5p directly targets ZEB1-AS1. Importantly, ZEB1-AS1 may act as an endogenous 'sponge' to regulate miRNA targets by competing for miR-181a-5p binding. In summary, our findings provide the evidence supporting the role of ZEB1-AS1 as an oncogene in CRC. Our study also demonstrates that miR-181a-5p targets not only protein-coding genes but also the lncRNA ZEB1-AS1.