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Non-small-cell lung cancer (NSCLC) is one of the deadliest cancers in the world. Circular RNA (circRNA) has been shown to participate in oncogenesis regulation, including lung cancer. Although the involvement of circRNAs in lung cancer has been reported, the regulatory mechanisms of circRNAs in NSCLC remain poorly understood. Thus, the present study aims at investigating the role of circARHGAP10 in NSCLC progression, which has been observed to be significantly upregulated in both NSCLC tissues and cell lines with profile analysis. A higher expression of circARHGAP10 also leads to a poor prognosis in NSCLC patients with fluorescence in situ hybridization (FISH). Both in vitro and in vivo experiments found that the downregulation of circARHGAP10 suppressed glycometabolism by decreasing GLUT1 expression. Silencing circARHGAP10 also suppressed proliferation and metastasis by targeting the miR-150-5p/GLUT1 axis in NSCLC, which was confirmed with a luciferase reporter assay. Overexpression of GLUT1 or downregulation miR-150-5p will recover NSCLC cell proliferation and metastasis after a knockdown of circARHGAP10. Taken together, these findings demonstrate that circARHGAP10 suppresses NSCLC progression by acting as a miR-150-5p sponge to promote GLUT1 expression. Thus, circARHGAP10 may be a potential target for NSCLC treatment. Keywords: circRNA ARHGAP10, miR-150-5p, GLUT-1, non-small-cell lung cancer, high-throughput RNA sequencing

To ascertain the inhibiting-frost ability of superhydrophobic surfaces, the processes of frosting and defrosting were observed on four surfaces with different microstructure topography-features in this work. Comparing with the untreated hydrophobic surface, the superhydrophobic microstructure surface exhibited superior anti-frosting performance. Besides, this work demonstrated that the anti-frosting property was sensitive to surface microscopic structure, since microstructures could induce to trap air pockets underneath the droplets to produce ultra-low water adhesion and thermal insulation, resulting in a significant delay of frost formation. After frost completely being melted into pure water, the superhydrophobic surfaces significantly contributed to enhance the defrosting efficiency and the coverage fraction of remained water was only 8.5% for microblock-nanohair hierarchical structure surface. The residual droplets in Cassie-Baxter state can be facilely removed by airflow or a slight inclination, whereas the melted water mostly firmly stayed on the flat untreated surface. In addition, the comparative researches with the other structure (i.e., microblock structures and nanohair structures) surfaces further ascertained that the nanostructures on the superhydrophobic surface will contribute to the coalescence movement of microdroplets, and the primary microstructures mainly play a role in jumping or sweeping movement of the coalesced droplets.

Emerging studies showed that α-hederin induced autophagic cell death in different cancers via reactive oxygen species. Nevertheless, α-hederin role in non-small-cell lung cancer (NSCLC) remains unknown. So, the aim of this study was to explain whether ferroptosis is a therapeutic strategy to NSCLC, and to explore the effect of α-hederin on NSCLC ferroptosis. Current investigation found that α-hederin inhibited NSCLC cell proliferation, invasion, and migration in vitro and in vivo at toxic doses. The α-hederin treatment also increased NSCLC cell chemosensitivity to cisplatin and promoted ferroptosis and apoptosis at a safe dose. Proteomics, metabolomics, and high-throughput sequencing detection confirmed that α-hederin treatment downregulated glutathione peroxidase 2 (GPX2), and glutathione synthase (GSS) expression suppressed the synthesis of glutathione (GSH), which destroyed the GSH redox system. Eventually, it led to ferroptosis, apoptosis, and membrane permeabilization in NSCLC. Taken together, the study provided molecular data to confirm that α-hederin induced ferroptosis, apoptosis, and membrane permeabilization in NSCLC by destroying the GSS/GSH/GPX2 axis-mediated GSH oxidation-reduction system at a safe and low-toxicity dose.

Chronic wounds are a common surgical problem exacerbated by diabetes. A hyperglycemic microenvironment induces inflammation and apoptosis, and plays an important role in vascular endothelial cell dysfunction in diabetes. Increasing evidence shows that high mobility group box 1 (HMGB1) expression is related to inflammation and apoptosis. The aim of this study was to determine the function of HMGB1 in hyperglycemia-induced vascular endothelial cell dysfunction. The results showed that the expression of HMGB1 was increased in human umbilical vein endothelial cells (HUVECs) after exposure to high glucose (25 mM). Downregulation of HMGB1 attenuated the high glucose-induced antiangiogenesis of HUVECs, and the decrease expression of HMGB1 inhibiting HUVEC apoptosis and inflammatory factor expression. In addition, miR-106 expression in HUVECs was decreased under high glucose conditions. Increased miR-106 significantly reversed the high glucose-induced vascular endothelial cell dysfunction by inhibition of HUVEC apoptosis and inflammatory factor expression. However, HMGB1 overexpression attenuated the protective effect of miR-106 on HUVECs in high glucose conditions. This suggested that miR-106 suppressed hyperglycemia-induced vascular endothelial cell dysfunction by targeting HMGB1. Double fluorescent reporter assays confirmed that miR-106 interacted with the 3′-UTR of HMGB1 and inhibited HMGB1 expression. Taken together, these data collectively suggested that miR-106 was a potential molecular target for inhibiting high glucose-induced inflammation and apoptosis by targeting HMGB1.

Icephobic/anti-icing materials have received growing attentions due to their great potential in reducing energy consumption. The aim of this presented work is to propose a superhydrophobic surface with microblock-nanohair hierarchical structures, and verify its water repellence and icephobic capacity. The hierarchical structures were fabricated by means of a combined method of electrochemical etching and hydrothermal treatment. Following this, the fluoridation modification was performed to obtain the superhydrophobicity with the water contact angle reaching 164° and the sliding angle of 1.5°. The dynamic droplet impacting on the hierarchical structure surface can rapidly rebounce off with the shorter contact time of 9.8 ms, displaying the robust dynamic water repellency. Comparing with the untreated substrate, the resultant superhydrophobic surface exhibited higher anti-icing property with the freezing time of a 4 μL reference droplet increasing from 11.3 s to ∼1700 s at −10 °C, and the ice adhesion force reducing to ∼35 kPa. Furthermore, the comparative studies with the other single-tier structure (i.e., microblock and nanohair structure) surfaces provided the necessary assistance to reveal the underlying action mechanism that the hierarchical micro-nanostructure induced more air pockets underneath droplets to produce the higher hydrophobicity and icephobic capacity.

This work introduces a facile method to fabricate a superhydrophobic aluminum surface with hierarchical micro-nanostructures based on a combination strategy of chemical etching and sand blasting. Comparing with the bare substrate, the micro-nanostructure superhydrophobic surface possessed an excellent resistance to wettability with water apparent contact angle as high as 160.2° and a low contact angle hysteresis of 6.7°. Also, it displayed a perfect bouncing dynamic of impact droplet with a short contact time of approximately 10 ms. Furthermore, the testing results of anti-icing and corrosion resistance indicated that the micro-nanostructure superhydrophobic surface was endowed with the robust anti-icing property and corrosion resistance. The freezing delay time was prolonged over 10 times comparing with that on the bare substrate, and the anti-frosting property was enhanced with the obviously decreased frosting area. Expectedly, the micro-nanostructure superhydrophobic surface was demonstrated to have a commendable resistance to corrosion, exhibiting a lower corrosion current density and a higher corrosion potential, as well as damage-free under 3.5 wt% NaCl salt spray environment. These investigations are believed that there is a certain extent promotion to applications of superhydrophobic surface, especially in the fields of anti-icing and corrosion prevention.

The aim of this paper is to report a facile strategy of planting a layer of petal shaped nanostructures on the surface of array micro-patterns, and producing the excellent superhydrophobicity and anti-icing property. In this work, the superhydrophobic surfaces were prepared by modifying petal shaped nanostructures (constructed by chemical etching in alkaline solution) planted on array micro-patterns (constructed by lithography process with the electrochemical etching under the neutral solution condition) on aluminum substrate with fluoroalkylsilane (FAS-17). Meanwhile, we further studied the effects of chemical etching process parameters on morphology and superhydrophobicity, and on this basis explored the anti-icing potential under the condition of icing wind tunnel. The results indicated that the process parameters including NaOH concentration of 0.05 M, etching time of 5 min, and the subsequent boiling time of 40 min were of benefit to producing the ideal nanostructure morphology and geometric dimension, and the resultant surface displayed an excellent superhydrophobicity with the apparent contact angle of 165° and the sliding angle being almost equal to zero (cannot be measured). Furthermore, the as-superhydrophobic surface generated a tremendous anti-icing potential, greatly preventing the icing accumulation at − 10 °C under the condition of icing wind tunnel, and exhibiting a lower ice adhesion strength comparing with a market mature production of superhydrophobic coating.

Solasonine is a compound isolated from Solanum melongena that has anti-infection properties, and promotes neurogenesis. However, the use of solasonine for the treatment of hepatocellular carcinoma (HCC) has not yet been reported. So, the aim of this study was to assess the efficacy of solasonine for the treatment of HCC. The effects of solasonine were tested using the HCC cell lines HepG2 and HepRG. Metabolomics analysis was conducted to assess the effects of solasonine on tumor growth of nude mice xenografts using HepG2 cells. The data demonstrated that solasonine significantly suppressed proliferation of HepG2 and HepRG cells. A mouse xenograft model of HepG2 tumor formation confirmed that solasonine suppressed tumor volume and weight, and inhibited HCC cell migration and invasion, as determined with the Transwell and scratch wound assays. To further reveal the underlying regulatory mechanism, metabolomics analysis was performed. The results revealed the effects of solasonine on glutathione metabolism, including glutathione peroxidase 4 (GPX4) and glutathione synthetase (GSS). The glutathione-dependent lipid hydroperoxidase GPX4 prevents ferroptosis by converting lipid hydroperoxides into non-toxic lipid alcohols. Ferroptosis has previously been implicated in the cell death that underlies several degenerative conditions, and induction of ferroptosis by the inhibition of GPX4 has emerged as a therapeutic strategy to trigger cancer cell death. Solasonine increased lipid ROS levels in HepG2 cells by suppression of GPX4 and GSS. However, the use of a ferroptosis inhibitor reversed solasonine-induced ROS production and cell apoptosis. Taken together, these results demonstrate that solasonine promotes ferroptosis of HCC cells via GPX4-induced destruction of the glutathione redox system.

Studying the causes of human–wildlife conflicts is important for reducing these conflicts. Human–wildlife conflicts can be divided into wild carnivore- and wild herbivore-related conflicts. Compared with carnivore-related conflicts, herbivore-related conflicts such as domestic livestock–wild herbivore conflicts (LHCs) have not been adequately studied, and there is scarce information on LHC intensity, causes, and impacts. LHCs frequently and extensively occur in the alpine ecosystem of the Chang Tang Plateau, China. Herbivorous wildlife competes with livestock for forage and habitat, which degrades the ecosystem, influences community livelihood, and decreases residents’ tolerance of wildlife. This study analyzed LHC causes in this plateau by focusing on forage competition, wild herbivore habitat and grazing land overlap using a comprehensive carrying capacity analysis method and niche Maxent model by integrating field surveys, statistical data, and remote sensing data. By integrating the domestic livestock with herbivorous wildlife into carrying capacity analysis, the stocking rate was 110%, which was 10% over the carrying capacity threshold. Overlap between wild herbivore habitat and domestic livestock grazing land was high, with Tibetan antelope ranging in 88% of the grazing land and domestic livestock grazing activities in 39.2% of Tibetan antelope habitat. Pasture fencing aggravated LHCs by fragmenting herbivore habitats and obstructing Tibetan antelope migration routes. LHCs in this plateau could be mitigated by extending the existing wildlife-related damage compensation scheme to cover wild herbivore-related damages, optimizing pasture fencing layout, diversifying community livelihood, and popularizing community-based wildlife management.