New insights for simultaneous nutrient removal enhancement and greenhouse gas emissions reduction of constructed wetland by optimizing its redox environment through manganese oxide addition.

Manganese oxide (MnOx) is receiving increased interest in the nutrient removal of constructed wetlands (CWs); however, its service effectiveness for simultaneous greenhouse gas (GHG) emissions reduction is still vague. In this study, three vertical flow CWs, i.e., volcanics (CCW), manganese sand uniformly mixing with volcanics (Mn-CW) and MnOx doped volcanics (MnV-CW), were constructed to investigate the underlying mechanisms of MnOx on nutrient removal enhancement and greenhouse gas (GHG) emissions reduction. The results showed that the MnOx doped volcanics optimized the oxidation-reduction potential surrounding the substrate (-164.0 ∼ +141.1 mv), and resulted in the lowest GHG emissions (CO2-equivalent) from MnV-CW, 16.8-36.5 % lower than that of Mn-CW and CCW. This was mainly ascribed to mitigation of N2O produced during the NO3--N reduction process, according to results of 15N stable isotope labeling. Analysis of the microbial community structure revealed that due to the optimized redox conditions through chemical doping of MnOx on volcanics, the abundance of microbe involved in denitrification and Mn-oxidizing process in the MnV-CW was significantly increased at genus level, which led to a higher Mn cycling efficiency between biogenic MnOx and Mn2+, and enhanced denitrification efficiency and N2O emission reduction. This study would help to understand and provide a preferable reference for future applications for manganese-based CW.

Efficient stabilization of arsenic migration and conversion in soil with surfactant-modified iron-manganese oxide: Environmental effects and mechanistic insights.

The use of iron-manganese oxide (FMO) as a promising amendment for remediating arsenic (As) contamination in soils has gained attention, but its application is limited owing to agglomeration issues. This study aims to address agglomeration using surfactant-modified FMO and investigate their stabilization behavior towards As and resulting environmental changes upon amendments. The results confirmed the efficacy of surfactants and demonstrated that cetyltrimethylammonium-bromide-modified FMO significantly reduced the leaching concentration of As by 92.5 % and effectively suppressed the uptake of As by 85.8 % compared with the control groups. The ratio of the residual fraction increased from 30.5-41.6 % in unamended soil to 67.9-69.2 %. The number of active sites was through the introduction of surfactants and immobilized As via complexation, ion exchange, and redox reactions. The study also revealed that amendments and the concentration of As influenced the soil physicochemical properties and enriched bacteria associated with As and Fe reduction and changed the distribution of C, N, Fe, and As metabolism genes, which promoted the stabilization of As. The interactions among cetyltrimethylammonium bromide, FMO, and microorganisms were found to have the greatest effect on As immobilization.

Natural product fargesin interferes with H3 histone lactylation via targeting PKM2 to inhibit non-small cell lung cancer tumorigenesis.

Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors. There is an urgent need to find more effective drugs that inhibit NSCLC. Fargesin (FGS) has demonstrated anti-tumor effects; however, its efficacy and the molecular mechanism of inhibiting NSCLC are unclear. Herein, we investigated FGS' inhibitory effects on NSCLC by CCK8 and EdU assays and cell cycle analysis of A549 cells in vitro and in a nude mouse tumor transplantation model in vivo. FGS (10-50 µM) significantly inhibited cell proliferation and down-regulated expression levels of CDK1 and CCND1. Transcriptomic analysis showed that FGS regulated the cell metabolic process pathway. Differential metabolites with FGS treatment were enriched in glycolysis and pyruvate pathways. Cell metabolism assay were used to evaluate the oxygen consumption rate (OCR), Extracellular acidification rate (ECAR) in A549 cells. FGS also inhibited the production of cellular lactate and the expression of LDHA, LDHB, PKM2, and SLC2A1. These genes were identified as important oncogenes in lung cancer, and their binding to FGS was confirmed by molecular docking simulation. Notably, the over-expression and gene silencing experiments signified PKM2 as the molecular target of FGS for anti-tumorigenesis. Moreover, the H3 histone lactylation, were correlated with tumorigenesis, were inhibited with FGS treatment. Conclusively, FGS inhibited the aerobic glycolytic and H3 histone lactylation signaling pathways in A549 NSCLC cells by targeting PKM2. These findings provide evidence of the therapeutic potential of FGS in NSCLC.

Releasing and Assessing the Toxicity of Polycyclic Aromatic Hydrocarbons from Biochar Loaded with Iron.

Iron (Fe)-loaded biochar has garnered attention for its potential applications in recent years. However, the pyrolysis process of Fe-loaded biochar generates polycyclic aromatic hydrocarbons (PAHs), which can have adverse effects on both human health and the environment. This study explored the correlation between Fe loading and PAH production in Fe-loaded biochar. The results indicate that increasing Fe loading in biochar reduces the PAH concentration, with the most significant decrease observed in naphthalene (0.02-0.08 mg/kg). This reduction can be attributed to the decrease in precursor compounds (e.g., C2H2), substitution of the C=O bond by Fe-O, and a decrease in the dissolved organic matter concentration (3.19-10.76 mg/L) with Fe loading. When Fe loading increased from 0 to 10%, the ecological toxicity of biochar increased by 33.48% due to an elevated production of dibenzo[a,h]anthracene, which poses a significant risk to human health. Therefore, it is imperative to take into consideration the ecological risk of PAHs prior to the application of Fe-loaded biochar. This study presents a comprehensive risk assessment of Fe-loaded biochar and provides valuable insights into the optimization of its production and safe application.

Highly efficient phosphorous removal in constructed wetland with iron scrap: Insights into the microbial removal mechanism.

Excessive phosphorus (P) in surface water can lead to serious eutrophication and economic losses. Iron-based constructed wetland (CW) is considered as a promising solution to eliminate P effectively due to the advantage of low-cost. However, there is limited available information on the microbial removal mechanism of P in iron-based CW up to now. Therefore, CW with iron scrap was constructed to investigate the treatment performance and microbial removal mechanism in this study. Results showed that efficient and stable P removal (97.09 ± 1.90%) was achieved in iron scrap-based CW during the experiment period, which was attributed to the precipitation of iron and P and improved microbially mediated P removal. Metagenomic analysis showed that microbial diversity was enhanced and phosphate accumulating organisms (e.g., Dechloromonas and Tetrasphaera) were enriched in CW with iron scrap, which explained higher P removal reasonably. In addition, the abundance of genes involved in the P starvation (e.g., phoB), uptake and transport (e.g., pstB) were enhanced in iron scrap-based CW. Enrichment analysis demonstrated that phosphotransferase pathway was also significantly up-regulated in CW with iron scraps, indicating that the energy supply of microbial P removal was enhanced. These findings provide a better understanding of the microbial removal mechanism of P in iron-based CW.

Enhancement of perfluorooctanoic acid and perfluorooctane sulphonic acid removal in constructed wetland using iron mineral: Performance and mechanisms.

Polyfluoroalkyl substance (PFAS) pose a threat to the aquatic environment due to their environmental persistence. The removal of PFAS using constructed wetlands (CWs) has received interest, but the adsorption saturation and limited removal capacity of the substrate is frequently challenging. To enhance the microbial degradation and performance of the substrate, different configurations of iron minerals were used as substrate to remove perfluorooctane sulphonic acid (PFOS) and perfluorooctanoic acid (PFOA) from CWs. The addition of iron minerals resulted in elimination of 57.2% and 63.9% of PFOS and PFOA in the effluent, respectively, which were 35.0% and 36.8% higher than that of control. Moreover, up to 85.4%, 86%, and 85.1% of NH4+, NO3-, and phosphorus, respectively, was removed using iron minerals. The enhanced electron transfer in iron mineral-based CWs was confirmed by a 61.2% increase in cytochrome C reductase content and an increased Fe(III)/Fe(II) ratio. Microbial analysis showed that the proportions of microbes with PFAS removal capacity (e.g. Burkholderiae and Pseudomonas), and the key pathways of the TCA cycle and glycolysis were increased in iron mineral-based CW. Based on these findings, we conclude that supplementation with iron mineral could enhance PFOA and PFOS removal in CWs.

Enhanced benzofluoranthrene removal in constructed wetlands with iron- modified biochar: Mediated by dissolved organic matter and microbial response.

Polycyclic aromatic hydrocarbons (PAHs) pose a high risk to ecosystems owing to their adverse environmental effects. The use of biochar in constructed wetlands (CWs) to remove PAH has received increased interest, but is frequently challenging because of saturation adsorption. To enhance the microbial degradation, electron acceptors are provided. This study aimed to remove a representative PAH, benzofluoranthrene (BbF), using iron-modified biochar as a supplement to the CW substrate. Results revealed that iron-mediated biochar based CWs increased the removal of BbF by 20.4 % and ammonium by 25.6 %. The BbF retained in substrate with biochar (36.6 % higher content) and further removed with iron modification (40.6 % lower content). Iron-modified biochar increased dissolved organic carbon content, particularly low-aromaticity, and low-molecular-weight organic matters (25.7 % higher tryptophan-like material), which contributed to PAH degradation by microorganisms. Microbial analysis confirmed that iron-mediated biochar enriched the abundance of microbes (e.g., Cellulomonas, Actinotalea, and Sphingomonas) and key enzymes (e.g., catA, lipV, and sdhA) that are involved in PAH degradation. Higher proportion of iron-reducing bacteria (e. g., Thiobacillus, Rhodobacter) played a significant role in driving microbial iron cycle, which was beneficial for PAHs removal. Based on the results, we confirmed that the use of iron-modified biochar in CWs enhance PAH removal.

CircP4HB regulates ferroptosis via SLC7A11-mediated glutathione synthesis in lung adenocarcinoma.

Background: Circular ribonucleic acids (circRNAs) play a key role in the development of different types of cancer. Ferroptosis is a type of programmed cell death that contributes to cancer progression. However, the role of circRNAs in lung adenocarcinoma (LUAD) ferroptosis remains unclear. Methods: The gene expression levels of circRNA P4HB (circP4HB), microRNA-1184 (miR-1184) and Solute carrier family 7 member 11 (Slc7a11), also known as Xct were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Ferroptosis of established LUAD cells was induced by erastin. Cell viability was examined via Cell Counting Kit 8 assays. Ferroptosis was evaluated by malondialdehyde (MDA), Prostaglandin-endoperoxide Synthase 2 (Ptgs2), lipid reactive oxygen species (lipid ROS), and JC-1 detection. The mechanism of circP4HB/miR-1184/SLC7A11 was investigated by luciferase reporter assays, RNA immunoprecipitation, RNA pull-down, and western blot assays. A functional for circP4HB in vivo was determined using xenograft nude mice models. Results: CircP4HB expression levels were increased in LUAD. It triggered glutathione (GSH) synthesis and, therefore protected LUAD cells from ferroptosis induced by erastin. CircP4HB may function as a competing endogenous RNA by modulating miR-1184 to regulate SLC7A11. CircP4HB inhibited ferroptosis by regulating miR-1184/ SLC7A11-mediated GSH synthesis. In vivo, overexpression of circP4HB promoted tumor growth and inhibited ferroptosis. Conclusions: The circRNA, circP4HB acts as a novel ferroptosis suppressor in LUAD. Furthermore, circP4HB protects LUAD from ferroptosis via modulation of the miR-1184/SLC7A11 axis. Our findings identified circP4HB as a novel biomarker in LUAD and warrants further investigation in the early diagnosis and treatment of LUAD.

Recent advances in application of iron-manganese oxide nanomaterials for removal of heavy metals in the aquatic environment.

Heavy metal pollution has a serious negative impact on the ecological environment and human health due to its toxicity, persistence, and non-biodegradable properties. Among the technologies applied in heavy metals removal, adsorption has been widely used as the most promising method because of its simple operation, high removal efficiency, strong applicability, and low cost. Iron-manganese oxide nanomaterials, as an effective absorbent, have attracted wide attention due to their simple preparation, wide material sources, and lower ecological impact. So far, no quantitative investigation has been conducted on the preparation and application of iron-manganese oxide nanomaterials in heavy metals removal. This review discussed the preparation methods and characteristics of iron­manganese oxide nanomaterials over the past decade and provided some basic information for the improvement of preparation methods. The physicochemical properties of iron­manganese oxide nanomaterials and environmental conditions are regarded as important factors that affect the removal efficiency of heavy metals. In addition, the removal mechanisms of heavy metals in aqueous solution with iron­manganese oxide nanomaterials were mainly included redox, complex precipitation, electrostatic attraction, and ion exchange. The reusability and practicability in actual wastewater treatment of 3nganese oxide nanomaterials were further discussed. Several key problems still need to be solved in the existing progress, such as improving the ability and stability of the iron­manganese oxide nanomaterials to remove heavy metals from actual wastewater. In conclusion, this review provides a future direction for the application of iron­manganese oxide nanomaterials for heavy metals removal and even in the large-scale treatment of actual wastewater.

MiR-937-3p promotes metastasis and angiogenesis and is activated by MYC in lung adenocarcinoma.

BACKGROUND: Non-small cell lung cancer (NSCLC) is still one of the diseases with the highest mortality and morbidity, and lung adenocarcinoma (LUAD) accounts for more than half of all NSCLC cases in most countries. miRNA can be used as a potential biological marker and treatment for lung adenocarcinoma. However, the effect of miR-937-3p to the invasion and metastasis of LUAD cells is not clear. METHODS: miRNA microarray is used to analyze the expression of miRNA in lung adenocarcinoma tissue. Transwell migration, Wound-healing assay and Western blot analysis are used to analyze cell migration, invasion and epithelial-mesenchymal transition (EMT) capabilities. Tube formation is used to assess angiogenesis ability. In addition, dual luciferase reporter gene detection is used to identify the potential binding between miRNA and target mRNA. In vivo experiments were performed on male NOD/SCID nude mice by tail vein injection to establish a transplanted tumor model. The CHIP experiment is used to verify the transcription factors of miRNA. RESULT: In our study, miR-937-3p was high-regulated in LUAD cell lines and tissues, and its expression level was related to tumor progression. We found that miR-937-3p high-expression has an effect on cell invasion and metastasis. In molecular mechanism, miR-937-3p causes SOX11 reduction by directly binding to the 3'-UTR of SOX11.In addition, MYC affects miR-937-3p transcription by binding to its promoter region. CONCLUSIONS: Our research shows that miR-937-3p is mediated by MYC and can control the angiogenesis, invasion and metastasis of LUAD by regulating SOX11, thereby promoting the progress of LUAD. We speculate that miR-937-3p can be used as a therapeutic target and potential biomarker for LUAD.

Tumor-derived exosomal miR-3157-3p promotes angiogenesis, vascular permeability and metastasis by targeting TIMP/KLF2 in non-small cell lung cancer.

Metastasis is the main cause of death in patients with advanced lung cancer. The exosomes released by cancer cells create tumor microenvironment, and then accelerate tumor metastasis. Cancer-derived exosomes are considered to be the main driving force for metastasis niche formation at foreign sites, but the mechanism in Non-small cell lung carcinoma (NSCLC) is unclear. In metastatic NSCLC patients, the expression level of miR-3157-3p in circulating exosomes was significantly higher than that of non-metastatic NSCLC patients. Here, we found that miR-3157-3p can be transferred from NSCLC cells to vascular endothelial cells through exosomes. Our work indicates that exosome miR-3157-3p is involved in the formation of pre-metastatic niche formation before tumor metastasis and may be used as a blood-based biomarker for NSCLC metastasis. Exosome miR-3157-3p has regulated the expression of VEGF/MMP2/MMP9 and occludin in endothelial cells by targeting TIMP/KLF2, thereby promoted angiogenesis and increased vascular permeability. In addition, exosome miR-3157-3p promoted the metastasis of NSCLC in vivo.

miR-550a-5p Functions as a Tumor Promoter by Targeting LIMD1 in Lung Adenocarcinoma.

Lung adenocarcinoma accounts for half of all lung cancer cases in most countries. Mounting evidence has demonstrated that microRNAs play important roles in cancer progression, and some of them can be identified as potential biomarkers. This study aimed to explore the role of miR-550a-5p, a lung adenocarcinoma-associated mature microRNA screened out from the TCGA database via R-studio and Perl, with abundant expression in samples and with 5-year survival prognosis difference, as well as having not been studied in lung cancer yet. Potential target genes were predicted by the online database. Gene ontology enrichment, pathway enrichment, protein-protein interaction network, and hub genes-microRNA network were constructed by FunRich, STRING database, and Cytoscape. Then, LIMD1, a known tumor suppressor gene reported by multiple articles, was found to have a negative correlation with miR-550a-5p. The expression of miR-550a-5p was up-regulated in tumor samples and tumor-associated cell lines. Its high expression was also correlated with tumor size. Cell line A549 treated with miR-550a-5p overexpression promoted tumor proliferation, while H1299 treated with miR-550a-5p knockdown showed the opposite result. Mechanically, miR-550a-5p negatively regulated LIMD1 by directly binding to its 3'-UTR validated by dual luciferase assay. In summary, a new potential prognostic and therapeutic biomarker, miR-550a-5p, has been identified by bioinformatics analysis and experimental validation in vitro and in vivo, which promotes lung adenocarcinoma by silencing a known suppressor oncogene LIMD1.

Circular RNA LPAR3 sponges microRNA-198 to facilitate esophageal cancer migration, invasion, and metastasis.

In this study, we explored expression and functions of circular RNA LPAR3 (circLPAR3) in esophageal squamous cell carcinoma (ESCC). The differential expression of circular RNAs (circRNAs) in 10 ESCC and corresponding paracarcinoma tissues was analyzed through circRNA microarray, then the candidate circRNAs were detected and verified through quantitative RT-PCR, and a novel circRNA was screened, which was circLPAR3. Circular RNA LPAR3 showed apparently high expression in ESCC tissues and cells, which was closely correlated with the clinical stage and lymph node metastasis of ESCC patients. Circular RNA LPAR3 was mainly located in the cytoplasm of ESCC cells, which was more stable than the baseline gene. Circular RNA LPAR3 upregulated MET gene expression through sponge adsorption of microRNA (miR)-198, activated the RAS/MAPK and the PI3K/Akt pathways, and promoted ESCC cell migration, invasion, and metastasis in vivo and in vitro. However, it had no effect on ESCC cell proliferation. Circular RNA LPAR3 can regulate the miR-198-MET signal axis to promote the migration, invasion, and metastasis of esophageal cancer cells, which can thereby serve as a potential diagnostic and therapeutic target of esophageal cancer.

hsa_circ_0006168 sponges miR-100 and regulates mTOR to promote the proliferation, migration and invasion of esophageal squamous cell carcinoma.

Circle RNAs (circRNAs) are the novel noncoding RNAs with the covalent closed-loop structure, which play a crucial role in a variety of pathological processes, including cancer. Nevertheless, the expression profiles and functions of circRNAs in esophageal squamous cell cancer (ESCC) remain largely unknown. In this paper, 10 pairs of ESCC tissues were utilized to screen the circRNA expression profiles by means of microarray assay; further, a novel circular RNA named hsa_circ_0006168 was investigated. Meanwhile, the expression of hsa_circ_0006168 was measured in 52 ESCC tissues and in cell lines. Our results suggested that, hsa_circ_0006168 was remarkably increased not only in ESCC tissues but also in cell lines compared with those in normal cases. Besides, high hsa_circ_0006168 expression was positively connected with lymph node metastasis and TNM stage of ESCC patients. In vitro, the proliferation, invasion and migration capacities of ESCC cells were suppressed through down-regulating hsa_circ_0006168 expression. Besides, RNase R digestion assay confirmed that hsa_circ_0006168 was more stable than its linear CNOT6L mRNA form. Moreover, nuclear and cytoplasmic fraction assay indicated that hsa_circ_0006168 was mainly distributed in the cytoplasm of Kyse450 and TE13 cells. Mechanically, it was discovered in this study that hsa_circ_0006168 might regulate the expression of Mammalian Target of Rapamycin (mTOR) by sponging microRNA-100 (miR-100). Taken together, hsa_circ_0006168 can promote ESCC proliferation, migration and invasion through the competing endogenous RNA (ceRNA) mechanism, which has been first confirmed in our results. In ESCC, hsa_circ_0006168 can serve as a potential diagnostic biomarker and therapeutic target.

Electrically Switched Ion Exchange Based on Carbon-Polypyrrole Composite Smart Materials for the Removal of ReO4- from Aqueous Solutions.

A simple and rapid process of ReO4- (as a surrogate of TcO4-) removal from aqueous solutions based on the electrically switched ion exchange (ESIX) method has been demonstrated in this work. Activated carbon-Polypyrrole (AC-PPy) was synthesized from activated carbon and pyrrole by electrodeposition method which was served as an electrically switched ion exchanger for ReO4- removal. The characterization results show that the AC-PPy composite exhibited an excellent loading capacity and a high stability for ions uptake and release. Chronoamperometric studies show that the ESIX treatment could be completed within 60 s, demonstrating the rapid uptake and release of ions. Uptake and release of ReO4- was verified by electrochemical quartz crystal microbalance with dissipation shift (EQCMD) studies. By modulating the electrochemical potential of the AC-PPy, the uptake and release of ReO4- ions can be controlled. Similar trends of uptake and release of ReO4- were observed in cyclic voltammetry (-0.4 to 0.8 V) for five cycles with the EQCMD. X-ray photoelectron spectroscopy (XPS) confirmed the process of ReO4- removal in the AC-PPy composite. Conclusively, the smart material shows excellent efficiency and selectivity for the removal of ReO4- from aqueous solutions.

MicroRNA-1204 promotes cell proliferation by regulating PITX1 in non-small-cell lung cancer.

MicroRNA-1204 (miR-1204), a member of the PVT1 region, may improve B cell differentiation and metastasis in breast cancer. However, the role of miR-1204 in non-small-cell lung cancer (NSCLC) and its mechanism remain unclear. The GEO public database was first employed to find differentially expressed genes. The expression level of miR-1204 in patient tissues and NSCLC cell lines was determined using qRT-PCR. Cell proliferation assays were performed to investigate the impact of miR-1204 on cell growth. Bioinformatics analysis and dual-luciferase reporter assays were conducted to find potential target genes. Finally, we performed in vivo experiments to identify the effect of miR-1204 on tumor formation in nude mice. It was first found that miR-1204 was overexpressed in NSCLC tissues and cells. miR-1204 increased the proliferation of NSCLC cells and reduced cell cycle arrest in vitro. PITX1 (paired like homeodomain 1) was found as a potential target gene. In addition, PITX1 was also found to be low in expression in NSCLC tissues and cells. To show that PITX1 reversed the function of miR-1204 in promoting proliferation, confirmatory experiments were performed. Moreover, high miR-1204 and low PITX1 expression was highly correlated with tumor size, lymph node metastasis, and the TNM stage in patients diagnosed with NSCLC. Our results suggested that upregulated miR-1204 in NSCLC is associated with NSCLC progression and promotes NSCLC cell proliferation by downregulating PITX1. miR-1204 may act as a poor prognostic factor and a potential therapeutic target for NSCLC.