Dioscin Impedes Proliferation, Metastasis and Enhances Autophagy of Gastric Cancer Cells via Regulating the USP8/TGM2 Pathway.

Gastric cancer (GC) is one of the most common cancers worldwide. Dioscin has been shown to have anti-cancer effects in GC. The aim of this study is to explore a novel mechanism of dioscin in repressing GC progression. Cell viability, proliferation, apoptosis and invasion were measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry and transwell assays, respectively. Monodansylcadaverine (MDC) staining was used to assess cell autophagy. The expression of transglutaminase-2 (TGM2), ubiquitin-specific peptidase 8 (USP8) and autophagy-related proteins was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. A xenograft tumor model was established to investigate the function of dioscin in vivo. Dioscin inhibited GC cell proliferation and invasion, but induced apoptosis and autophagy. TGM2 was highly expressed in GC, and dioscin suppressed GC progression by decreasing the protein level of TGM2. Furthermore, USP8 positively regulated TGM2 expression, and TGM2 overexpression reversed the inhibitory effect of USP8 knockdown on GC cell progression. USP8 abated the effect of dioscin in GC cells. Dioscin decreased the protein level of TGM2 via regulating USP8. In addition, dioscin restrained GC tumor growth in vivo. Dioscin played an anti-cancer effect in GC by enhancing cancer cell autophagy via regulating the USP8/TGM2 pathway.

Schizandrin A induces the apoptosis and suppresses the proliferation, invasion and migration of gastric cancer cells by activating endoplasmic reticulum stress.

Apart from its basic antioxidant and anti­inflammatory properties, schizandrin A (SchA), which is isolated from Fructus schisandra, can exert anticancer effects on multiple cancer types. However, to the best of our knowledge, there has been no study identifying the impacts of SchA on gastric cancer (GC). Therefore, the aim of the present study was to identify how SchA functioned to affect the progression of GC. To investigate the role of SchA in GC development, Cell Counting Kit­8, colony formation, wound healing and Transwell assays were conducted to assess the viability, proliferation, migration and invasion of AGS cells, respectively. Then, the apoptosis rate and apoptosis­ and endoplasmic reticulum (ER) stress­related protein expression levels in AGS cells exposed to SchA were detected via TUNEL assays and western blotting, respectively. Subsequently, the aforementioned functional assays were performed again in AGS cells exposed to both SchA and the ER stress inhibitor 4­phenylbutyric acid (4­PBA) for the confirmation of the effect of SchA on ER stress in GC. It was found that SchA markedly decreased the viability, proliferation, migration and invasion, while it induced the apoptosis of AGS cells. Moreover, the markers of ER stress were elevated by SchA treatment in AGS cells. Nevertheless, 4­PBA reversed the effects of SchA on the viability, proliferation, migration, invasion and apoptosis of AGS cells, accompanied by decreased expression of ER stress markers. In conclusion, the present study demonstrated that SchA induced the apoptosis and suppressed the proliferation, invasion and migration of GC cells by activating ER stress, which provides a theoretical basis for the use of SchA in the treatment of GC.

Facile Strategy to Fabricate the Flame Retardant Polyamide 66 Fabric Modified with an Inorganic-Organic Hybrid Structure.

Recently, traditional flame retardant finishing with a single metal compound has been rarely applied owing to its low effectiveness and durability. This study reports metal ion finishing in combination with surface photografting modification (M/P technology) as a novel approach to incorporate an inorganic-organic hybrid structure containing an Fe3+ ion onto the surface of the polyamide (PA) 66 fabric. Specifically, the PA fabric was first surface-modified in the presence of acrylic acid (AA) and N,N'-methylene bisacrylamide (MBAAn) during photografting pretreatment under UV irradiation (step I), then further reacted with the Fe3+ ion in the metal ion finishing (step II). After treatment with M/P technology, the fabric exhibits the required excellent flame retardancy and dripping resistance. Here, flame retardant tests show that the treated PA fabric has the highest limiting oxygen index (LOI) value of 33.4 and no melt dripping during combustion. An interesting inorganic/organic composite thermal barrier consisting of an inorganic iron oxide nanoparticle (NP) outer layer and an organic micro-intumescent inner layer can be observed on the surface of the burnt fabric. This structure could be responsible for the significant enhancement in the fire performance of the treated fabric. Importantly, the treated fabric is also highly stable during the laundering procedure, which could retain a high Fe/C ratio and an acceptable LOI value of 27.8 after washing 45 times. This confirms the achievement of durable flame retardancy after treatment with M/P technology, and its possible interaction mechanism has been discussed here.

Down-regulation of G protein-coupled receptor 137 by RNA interference inhibits cell growth of two hepatoma cell lines.

G protein-coupled receptors (GPCRs) are important signal transduction mediators and pharmacological therapeutic targets. G protein-coupled receptor 137 (GPR137) was initially reported as a novel orphan GPCR around 10 years ago. Some orphan GPCRs have been implicated in cancer cell proliferation and migration. The aim of this study is to investigate the role of GPR137 in hepatocellular carcinoma (HCC). GPR137 is widely expressed in several human HCC cell lines, as determined by real-time PCR. We then applied lentivirus mediated RNA interference (RNAi) to knock down GPR137 expression in two HCC cell lines HepG2 and Bel7404. Depletion of GPR137 remarkably inhibited cell proliferation and colony formation capacity. Knockdown of GPR137 in HepG2 cells led to cell cycle arrest at G0/G1 phase and G2/M phase, and induced cell apoptosis, as determined by flow cytometry analysis, which contributed to cell growth inhibition. Our findings suggested that GPR137 could facilitate HCC cell proliferation and thus promote hepatocarcinogenesis.

Double In Situ Approach for the Preparation of Polymer Nanocomposite with Multi-functionality.

A novel one-step synthetic route, the double in situ approach, is used to produce both TiO(2) nanoparticles and polymer (PET), and simultaneously forming a nanocomposite with multi-functionality. The method uses the release of water during esterification to hydrolyze titanium (IV) butoxide (Ti(OBu)(4)) forming nano-TiO(2) in the polymerization vessel. This new approach is of general significance in the preparation of polymer nanocomposites, and will lead to a new route in the synthesis of multi-functional polymer nanocomposites.