Efficient composite chlorinated ethenes removal using gallic acid to enhance Fe/Ni nanoparticles activated persulfate.

As the representative volatile chlorinated hydrocarbons detected in wastewater, the removal of composite chlorinated ethenes is a major challenge in wastewater treatment. In the present study, an efficient removal system for composite chlorinated ethenes was reported, in which gallic acid was used to enhance the activation of persulfate by Fe/Ni nanoparticles. The influences of gallic acid-Fe/Ni and persulfate concentrations, initial pH value, reaction temperature, inorganic anions, and natural organic matters were evaluated in the composite chlorinated ethenes removal. Our results showed that the gallic acid-Fe/Ni-persulfate system with 9.0 mM of gallic acid-Fe/Ni and 30.0 mM of persulfate yielded about 100% trichloroethylene removal and 97.3%-98.6% perchloroethylene removal in the pH range of 3.0-12.0. Electron paramagnetic resonance analysis and radical quenching experiments indicated that SO4•- and •OH were the predominant radical species under acidic and alkaline conditions. Ultraviolet visible spectroscopy and inductively coupled plasma optical emission spectrometer tests revealed the Fe-gallic acid chelation could regulate the concentration of iron ions and improve the reactivity of gallic acid-Fe/Ni. These results demonstrated that the gallic acid-Fe/Ni-persulfate system was a promising strategy for treating composite chlorinated ethenes-containing wastewater.

Tannic acid promotes the activation of persulfate with Fe(ii) for highly efficient trichloroethylene removal.

Trichloroethylene (TCE) is an Environmental Protection Agency (EPA) priority pollutant that is difficult to be removed by some remediation methods. For instance, TCE removal using persulfate (PS) activated by ferrous iron (Fe(ii)) has been tested but is limited by the unstable Fe(ii) concentration and the initial pH of contaminated water samples. Here we reported a new TCE removal system, in which tannic acid (TA) promoted the activation of PS with Fe(ii) (TA-Fe(ii)-PS system). The effect of initial pH, temperature, and concentrations of PS, Fe(ii), TA, inorganic anions and humic acid on TCE removal was investigated. We found that the TA-Fe(ii)-PS system with 80 mg L-1 of TA, 1.5 mM of Fe(ii) and 15 mM of PS yielded about 96.2-99.1% TCE removal in the pH range of 1.5-11.0. Radical quenching experiments were performed to identify active species. Results showed that SO4˙- and ˙OH were primarily responsible for TCE removal in the TA-Fe(ii)-PS system. In the presence of TA, the Fe-TA chelation and the reduction of TA could regulate Fe(ii) concentration and activate persulfate for continuously releasing reactive species under alkaline conditions. Based on the excellent removal performance for TCE, the TA-Fe(ii)-PS system becomes a promising candidate for controlling TCE in groundwater.

SP1-induced overexpression of LINC00520 facilitates non-small cell lung cancer progression through miR-577/CCNE2 pathway and predicts poor prognosis.

Long noncoding RNAs (lncRNAs) have gained much attention in the past few years. Long intergenic non-protein coding RNA 520 (LINC00520) was one of the newly discovered lncRNA which has been demonstrated to be dysregulated in several cancers. So far, the function and mechanism of LINC00520 in non-small cell lung cancer (NSCLC) are unclear. In this paper, our group first showed that LINC00520 level was elevated in non-small cell lung cancer (NSCLC) tissue and cells. In addition, SP1 could bind directly to the promoter region of LINC00520 and thus promote its transcription. Increased LINC00520 was distinctly correlated with advanced tumor stage and shorter survival time in NSCLC patients. Further functional investigations provided evidences that forced down regulation of LINC00520 inhibited NSCLC cell proliferation, invasion, metastasis and EMT, while contributing to cells apoptosis. Mechanistically, we found that LINC00520 serving as a competing endogenous RNA to be involved in the modulation of miR-577 expressions, and thus affected the expression of CCNE2 which was a target gene of miR-577. Moreover, in NSCLC cells with si-LINC00520, up regulation of CCNE2 led to an increase of cell growth and invasion. Taken together, LINC00520 displayed its tumor-promotive roles through modulating the miR-577/CCNE2 axis, highlighting a potential therapeutic strategy for NSCLC patients.

The Impact of High-mobility Group Box Mutation of T-cell Factor 4 on Its Genomic Binding Pattern in Non-small Cell Lung Cancer.

T-cell factor 4 (TCF-4) is determined to play a crucial role in Wnt/ß-catenin signaling pathway activation. The mutations and alternative splice isoforms of TCF-4 can cause cancers and other diseases. The high-mobility group (HMG) box domain of TCF-4 contributes to interacting with DNA motif for transcriptional regulation. However, the impact of the mutations within HMG box of TCF-4 on the genomic binding pattern is poorly investigated. Herein, we generated non-small cell lung cancer (NSCLC) cell line A549 with stably overexpressed TCF-4 with HMG box hot spot mutation (10th exon partial deletion), and conducted TCF-4 and ß-catenin chromatin immunoprecipitation sequence to explore the differential genomic binding patterns. Our results revealed that TCF-4 lost 19365 but gained 1724 peaks, and ß-catenin lost 4035 but gained 5287 peaks upon mutant TCF-4 compared with the wild type (log2FC > 1 or < -1, FDR<0.01). The transcriptional levels of the genes associated with these differential peaks such as H3F3C, KRT1, KRT14, MMp1, and MMP15 were all found to strongly change responding to TCF-4 binding (P < 0.05). Furthermore, A549 cells with TCF-4 mutation displayed a more compromising tumor characterization on cell proliferation and invasion. Our data determined the important role of TCF-4 in gene transcription controlling and provided the gain function evidence of TCF-4 caused by the TCF-4 mutation in NSCLC.

Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC-5 cells by up-regulation of miR-103.

The beneficial function of gastrodin towards many inflammatory diseases has been identified. This study designed to see the influence of gastrodin in a cell model of chronic obstructive pulmonary disease (COPD). MRC-5 cells were treated by LPS, before which gastrodin was administrated. The effects of gastrodin were evaluated by conducting CCK-8, FITC-PI double staining, Western blot, qRT-PCR and ELISA. Besides this, the downstream effector and signalling were studied to decode how gastrodin exerted its function. And dual-luciferase assay was used to detect the targeting link between miR-103 and lipoprotein receptor-related protein 1 (LRP1). LPS induced apoptosis and the release of MCP-1, IL-6 and TNF-α in MRC-5 cells. Pre-treating MRC-5 cells with gastrodin attenuated LPS-induced cell damage. Meanwhile, p38/JNK and NF-κB pathways induced by LPS were repressed by gastrodin. miR-103 expression was elevated by gastrodin. Further, the protective functions of gastrodin were attenuated by miR-103 silencing. And LRP1 was a target of miR-103 and negatively regulated by miR-103. The in vitro data illustrated the protective function of gastrodin in LPS-injured MRC-5 cells. Gastrodin exerted its function possibly by up-regulating miR-103 and modulating p38/JNK and NF-κB pathways.