RESUMO
The objective of this study is to unravel the modification mechanism of a coupling agent on the water sensitivity of phosphogypsum asphalt mortar. The adhesion process of phosphogypsum asphalt mastic modified with three kinds of coupling agents (KH-550, KH-570, and CS-101) and raw phosphogypsum to the aggregate minerals was simulated based on the molecular dynamics software, Materials Studio 2020, and the water film layer was considered along the simulation. When the three coupling agents were added, the interfacial adhesion work gradually increased with the increase of modified phosphogypsum dosage, and the trends of each model were relatively similar. With the increase of simulation time, the mean square displacement of water molecules of the three interfacial models showed different trends, and the increasing trend rank was unmodified phosphogypsum > KH-550 > KH-570 > CS-101. The diffusion coefficient of the water molecular layer of asphalt mastic modified with CS-101 coupling agent in phosphogypsum shows a significant decrease with the increase of CS-101-modified phosphogypsum (more than 5% mass ratio to asphalt). Compared to raw phosphogypsum asphalt mortar, the addition of coupling agents can significantly limit the diffusion of water molecules and effectively improve the interfacial adhesion work, in which CS-101 coupling agent has the best effect, followed by KH-570 and KH-550.
RESUMO
The morbidity and mortality of hepatocellular carcinoma (HCC) are growing yearly. Several reports emphasize the importance of long non-coding RNAs (lncRNAs) in HCC. This paper provides a molecular mechanism for the function of GAS6-AS2 in HCC. The expressions of GAS6-AS2, miR-493-5p and OTUB1 were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were measured by cell counting kit-8 (CCK-8), flow cytometry and transwell assay, respectively. The interaction of miR-493-5p and GAS6-AS2 or OTU domain-containing Ubiquitin Aldehyde-binding Protein 1 (OTUB1) was analyzed by starBase v2.0 and verified by luciferase reporter assay. The protein level of OTUB1 as well as PI3K, p-PI3K, AKT, p-AKT, FoxO3a, p-FoxO3a and ß-actin protein levels were distinguished by western blot. GAS6-AS2 was up-regulated in HCC tissues and cells. GAS6-AS2 knockdown inhibited proliferation, migration, and invasion but promoted apoptosis. MiR-493-5p, a target of GAS6-AS2, was down-regulated in HCC tissues and cells. Inhibition of miR-493-5p reversed the effects of GAS6-AS2 knockdown on HCC cells. OTUB1, a target of miR-493-5p, was up-regulated in HCC cells and its expression was modulated by miR-493-5p. Overexpression of OTUB1 recovered the positive effects of miR-493-5p enrichment or GAS6-AS2 knockdown on HCC cells. GAS6-AS2 knockdown impeded the activation of PI3K/AKT/FoxO3a signaling pathway, while this activation was reversed by miR-493-5p inhibition or OTUB1 overexpression. In conclusion, GAS6-AS2 knockdown suppressed proliferation, migration, and invasion but promoted apoptosis of HCC cells by impeding PI3K/AKT/FoxO3a signaling pathway through regulating the GAS6-AS2/miR-493-5p/OTUB1 axis.
