MOESM1 of Green synthesis of enzyme/metal-organic framework composites with high stability in protein denaturing solvents

Additional file 1. Additional information

MOESM1 of Green synthesis of enzyme/metal-organic framework composites with high stability in protein denaturing solvents

Additional file 1. Additional information

Interleukin 17A Promotes Gastric Cancer Invasiveness via NF-κB Mediated Matrix Metalloproteinases 2 and 9 Expression

<div><p>Interleukin 17A (IL-17A), as a pro-inflammatory cytokine, is involved in pathology of inflammatory diseases and tumor microenvironment. The aim of this study is to investigate the effect of IL-17A on the invasiveness of gastric cancer (GC). In the study, we found that IL-17A could promote the migration and invasion of GC cells. Furthermore, after treated with IL-17A, the expressions and activities of matrix metalloproteinase 2 (MMP-2) and MMP-9 were upregulated, while the expressions of TIMP-1 and TIMP-2 were downregulated. Moreover, the nuclear/overall fractions of p65 and p50 were dramatically elevated by IL-17A. Pretreatment with helenalin, a nuclear factor-κB (NF-κB) inhibitor, was proved to abolish the promoting effect of IL-17A on the invasion ability of GC cells and upregulation of MMP-2 and MMP-9. In conclusion, our findings illustrated that IL-17A could promote the invasion of GC cells by activating NF-κB pathway, and subsequently upregulating the expression of MMP-2 and MMP-9. These results may lead to the identification of new diagnostic markers and therapeutic targets of GC.</p></div

IL-17A activates NF-κB pathway in AGS cells.

<p>(A) Western blotting analysis was used to detect overall p50, p65, p52, c-Rel and RelB expression in AGS cells treated with IL-17A (50 ng/ml) at indicated time points. (B) Quantification of the protein levels of overall p50, p65, p52, c-Rel and RelB. (C) Western blotting analysis was used to detect nuclear p50, p65, p52, c-Rel and RelB expression in AGS cells treated with IL-17A (50 ng/mL) at indicated time points. (D) Quantification of the protein levels of nuclear p50, p65, p52, c-Rel and RelB. (E) The relative ratio of nuclear to overall fraction of p50, p65, p52, c-Rel and RelB. Values represent the means ± SD of three independent experiments performed in triplicate. **<i>p</i><0.01, compared with the control group.</p

IL-17A promotes gastric cancer cell migration and invasion.

<p>(A) IL-17A treated GC cells (AGS, BGC-823 and SGC-7901) showed higher motility in a wound-healing assay, compared with cells without IL-17A treatment. (B) The percent migration rate is expressed as a percentage of the beginning area. (C) Effect of IL-17A on cell invasion was detected by transwell assay. Representative pictures of cells migrated through Matrigel-coated transwell were shown. (D) Total invasive cell number in each chamber was summarized as a percentage of control. Values represent the means ± SD of three independent experiments performed in triplicate. *<i>p</i><0.05 and **<i>p</i><0.01 compared with the control group.</p

Effects of the NF-κB inhibitor and IL-17A on cell invasion and the expressions of MMP-2 and MMP-9 in AGS cells.

<p>(A) 1×10⁶ AGS cells were pretreated with helenalin (5 µM) for 30 min and then incubated in the presence or absence of IL-17A (50 ng/ml) for 24 h. Cellular invasiveness was measured using the transwell invasion assay. (B) The percent invasion rate was expressed as a percentage of control. (C, D) AGS cells were treated and then subjected to western blotting to analyze the protein levels of MMP-2 and MMP-9. Values represent the means ± SD of three independent experiments performed in triplicate. *<i>p</i><0.05 and **<i>p</i><0.01 compared with the control group.</p

IL-17A promotes the expressions and activities of MMP-2 and MMP-9 and suppresses the expressions of TIMP-1 and TIMP-2 in gastric cancer cells.

<p>(A) Expressions of MMPs in GC cells (AGS and BGC-823) were compared by western blotting between cells treated with and without IL-17A (50 ng/ml) for 24 h. (B) Quantification of the protein levels of MMP-2 and MMP-9. (C) Effects of IL-17A on the activities of MMP-2 and MMP-9. (D) Quantification of the activities of MMP-2 and MMP-9. Values represent the means ± SD of three independent experiments performed in triplicate. *<i>p</i><0.05 and **<i>p</i><0.01 compared with the control group.</p

DataSheet_1_Heme oxygenase-1 modulates ferroptosis by fine-tuning levels of intracellular iron and reactive oxygen species of macrophages in response to Bacillus Calmette-Guerin infection.pdf

Macrophages are the host cells and the frontline defense against Mycobacterium tuberculosis (Mtb) infection, and the form of death of infected macrophages plays a pivotal role in the outcome of Mtb infections. Ferroptosis, a programmed necrotic cell death induced by overwhelming lipid peroxidation, was confirmed as one of the mechanisms of Mtb spread following infection and the pathogenesis of tuberculosis (TB). However, the mechanism underlying the macrophage ferroptosis induced by Mtb infection has not yet been fully understood. In the present study, transcriptome analysis revealed the upregulation of heme oxygenase-1 (HMOX1) and pro-ferroptosis cytokines, but downregulation of glutathione peroxidase 4 (GPX4) and other key anti-lipid peroxidation factors in the peripheral blood of both patients with extra-pulmonary tuberculosis (EPTB) and pulmonary tuberculosis (PTB). This finding was further corroborated in mice and RAW264.7 murine macrophage-like cells infected with Bacillus Calmette-Guerin (BCG). A mechanistic study further demonstrated that heme oxygenase-1 protein (HO-1) regulated the production of reactive oxygen species (ROS) and iron metabolism, and ferroptosis in BCG-infected murine macrophages. The knockdown of Hmox1 by siRNA resulted in a significant increase of intracellular ROS, Fe2+, and iron autophagy-mediated factor Ncoa4, along with the reduction of antioxidant factors Gpx4 and Fsp1 in macrophages infected with BCG. The siRNA-mediated knockdown of Hmox1 also reduced cell survival rate and increased the release of intracellular bacteria in BCG-infected macrophages. By contrast, scavenging ROS by N-acetyl cysteine led to the reduction of intracellular ROS, Fe2+, and Hmox1 concentrations, and subsequently inhibited ferroptosis and the release of intracellular BCG in RAW264.7 cells infected with BCG. These findings suggest that HO-1 is an essential regulator of Mtb-induced ferroptosis, which regulates ROS production and iron accretion to alter macrophage death against Mtb infections.</p

Influence of Capillary Effects on Electric Response of Well-Ordered Carbon Nanotube Film

The interface structure in nanocomposite materials often directly influences the electric, thermal, and mechanical properties of functional architectures and limits their application in many fields, in addition to the characteristics of their nanobuilding blocks. In this work, we report that the electronic transport characteristic of a well-ordered carbon nanotube film is adjusted by the structural evolution of the junction caused by capillary effects. This mechanism can explain the resistance change and recovery throughout the immersion–evaporation process and even the anomalous transient decrease in the resistance. Meanwhile, we establish a relationship between the resistance change ratio of the film and the interfacial tension between the film and the immersion liquid. The ability to achieve a sensitive and repeatable resistance change in a carbon nanotube film could have important implications in the measurement of liquid properties, liquid sensors, and solution analysis and provide a new avenue for the development of new multifunctional architectures

Additional file 1: of Prolonged inhibition of class I PI3K promotes liver cancer stem cell expansion by augmenting SGK3/GSK-3β/β-catenin signalling

Table S1. Primer sequences for quantitative RT-PCR. (DOCX 24 kb