Improvement of biotic nitrate reduction in constructed photoautotrophic biofilm-soil microbial fuel cells.

The biotic nitrate reduction rate in freshwater ecosystems is typically constrained by the scarcity of carbon sources. In this study, 'two-chambers' - 'two-electrodes' photoautotrophic biofilm-soil microbial fuel cells (P-SMFC) was developed to accelerate nitrate reduction by activating in situ electron donors that originated from the soil organic carbon (SOC). The nitrate reduction rate of P-SMFC (0.1341 d-1) improved by âˆ¼ 1.6 times on the 28th day compared to the control photoautotrophic biofilm. The relative abundance of electroactive bacterium increased in the P-SMFC and this bacterium contributed to obtain electrons from SOC. Biochar amendment decreased the resistivity of P-SMFC, increased the electron transferring efficiency, and mitigated anodic acidification, which continuously facilitated the thriving of putative electroactive bacterium and promoted current generation. The results from physiological and ecological tests revealed that the cathodic photoautotrophic biofilm produced more extracellular protein, increased the relative abundance of Lachnospiraceae, Magnetospirillaceae, Pseudomonadaceae, and Sphingomonadaceae, and improved the activity of nitrate reductase and ATPase. Correspondingly, P-SMFC in the presence of biochar achieved the highest reaction rate constant for nitrate reduction (kobs) (0.2092 d-1) which was 2.4 times higher than the control photoautotrophic biofilm. This study provided a new strategy to vitalize in situ carbon sources in paddy soil for nitrate reduction by the construction of P-SMFC.

Using the sulfide-oxidizing bacterium Geobacillus thermodenitrificans to restrict H2S release during chicken manure composting.

Hydrogen sulfide (H2S) is a toxic gas massively released during chicken manure composting. Diminishing its release requires efficient and low cost methods. In recent years, heterotrophic bacteria capable of rapid H2S oxidation have been discovered but their applications in environmental improvement are rarely reported. Herein, we investigated H2S oxidation activity of a heterotrophic thermophilic bacterium Geobacillus thermodenitrificans DSM465, which contains a H2S oxidation pathway composed by sulfide:quinone oxidoreductase (SQR) and persulfide dioxygenase (PDO). This strain rapidly oxidized H2S to sulfane sulfur and thiosulfate. The oxidation rate reached 5.73 µmol min-1·g-1 of cell dry weight. We used G. thermodenitrificans DSM465 to restrict H2S release during chicken manure composting. The H2S emission during composting process reduced by 27.5% and sulfate content in the final compost increased by 34.4%. In addition, this strain prolonged the high temperature phase by 7 days. Thus, using G. thermodenitrificans DSM465 to control H2S release was an efficient and economic method. This study provided a new strategy for making waste composting environmental friendly and shed light on perspective applications of heterotrophic H2S oxidation bacteria in environmental improvements.

Improved NH3 Uptake of a Macromolecule-Metal Complex Constructed with Dual Polymeric Ligands and M(II).

MOFs are considered as efficient NH3 adsorbents for their high capacity but are accompanied by the collapse of MOFs. In this work, macromolecule-metal complexes (MMCs), which could provide metal sites like MOFs, were developed for reversible NH3 uptake with high capacity with the assistance of the polymeric ligands. Based on the tunable structure of MMCs, the role of the polymeric ligands and metallic center was investigated. Thereinto, MMCs-3 with dual polymeric ligands presented higher NH3 adsorption capacity and reversibility of adsorbents compared with MMCs containing a single polymeric ligand (MMCs-1 and MMCs-2). Combined with the NH3 adsorption test, characterization of FT-IR, UV-vis, EPR spectroscopy, NH3-TPD measurement, and the DFT calculations, it was found that the neutral polymeric ligands PVIm contributed to improve the stability of MMCs-3 under a NH3 atmosphere for the tough networks of PVIm-M(II), while the polymeric ligands with a carboxylate anion together with M(II) enhanced the NH3 capacity for the feasible coordination of a carboxylate anion with M(II). The mechanism of NH3 uptake by PVIm-Co-PVBA was proposed that the NH3 was fixed through the coordination with Co(II) along with the departure of PVBA and the following hydrogen bonding interaction with PVBA, while the coordination between PVIm and Co(II) was not destroyed. Thus, MMCs-3 with dual polymeric ligands presented a higher NH3 uptake capacity and stability. Optimally, PVIm-M-PVBA with the metal center of Co(II), Cu(II), and Ni(II) were obtained with a high capacity of 20.8-23.7 NH3 mmol/g at 25 °C and 1 bar and a high selectivity of NH3 over CO2 (54.9-99.9) and N2 (73.0-187.6) through the breakthrough measurement with a gas mixture of 0.2% NH3, 2% CO2, and 99.6% N2 at 25 °C.

[Corrigendum] Long non­coding RNA AC245100.4 promotes prostate cancer tumorigenesis via the microRNA­145­5p/RBBP5 axis.

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the cell proliferation and migration assay data shown in Figs. 6D and 7B, there were a pair of panels showing overlapping data, such that the same data had apparently been selected to show the results from different experiments. Subsequently, the authors referred back to their original data, and identified further incorrectly assembled data panels in Figs. 3B and 7B. The corrected versions of Fig. 3B (showing the correct data for the 'AC245100.4 / PC3 / 0 h' scratch­wound assay data panel), Fig. 6D (showing the correct data for the 'PC3 / NC­mimic' and 'DU­145 / NC­inhibitor' data panels) and Fig. 7D (showing the correct data for the 'PC3 / 24 h / Inhibitor­miR­145­5p + siAC245100.4' data panel) are shown on the subsequent pages. The authors regret the errors that were made during the preparation of the published figures, and confirm that these errors did not grossly affect the conclusions reported in the study. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 45: 619­629, 2021; DOI: 10.3892/or.2020.7894].

iORbase: A database for the prediction of the structures and functions of insect olfactory receptors.

Insect olfactory receptors (iORs) with atypical 7-transmembrane domains, unlike Chordata olfactory receptors, are not in the GPCR protein family. iORs selectively bind to volatile ligands in the environment and affect essential insect behaviors. In this study, we constructed a new platform (iORbase, https://www.iorbase.com) for the structural and functional analysis of iORs based on a combined algorithm for gene annotation and protein structure prediction. Moreover, it provides the option to calculate the binding affinities and binding residues between iORs and pheromone molecules by virtual screening of docking. Furthermore, iORbase supports the automatic structural and functional prediction of user-submitted iORs or pheromones. iORbase contains the well-analyzed results of approximately 6 000 iORs and their 3D protein structures identified from 59 insect species and 2 077 insect pheromones from the literature, as well as approximately 12 million pairs of simulated interactions between functional iORs and pheromones. We also built 4 online modules, iORPDB, iInteraction, iModelTM, and iOdorTool to easily retrieve and visualize the 3D structures and interactions. iORbase can help greatly improve the experimental efficiency and success rate, identify new insecticide targets, or develop electronic nose technology. This study will shed light on the olfactory recognition mechanism and evolutionary characteristics from the perspectives of omics and macroevolution.

Parthenolide reveals an allosteric mode to inhibit the deISGylation activity of SARS-CoV­2 papain-like protease.

The coronavirus papain-like protease (PLpro) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for viral polypeptide cleavage and the deISGylation of interferon-stimulated gene 15 (ISG15), which enable it to participate in virus replication and host innate immune pathways. Therefore, PLpro is considered an attractive antiviral drug target. Here, we show that parthenolide, a germacrane sesquiterpene lactone, has SARS-CoV-2 PLpro inhibitory activity. Parthenolide covalently binds to Cys-191 or Cys-194 of the PLpro protein, but not the Cys-111 at the PLpro catalytic site. Mutation of Cys-191 or Cys-194 reduces the activity of PLpro. Molecular docking studies show that parthenolide may also form hydrogen bonds with Lys-192, Thr-193, and Gln-231. Furthermore, parthenolide inhibits the deISGylation but not the deubiquitinating activity of PLpro in vitro. These results reveal that parthenolide inhibits PLpro activity by allosteric regulation.

Expression and prognosis of CDC45 in cervical cancer based on the GEO database.

Cervical cancer is one of the most common malignant tumors in women, and its morbidity and mortality are increasing year by year worldwide. Therefore, an urgent and challenging task is to identify potential biomarkers for cervical cancer. This study aims to identify the hub genes based on the GEO database and then validate their prognostic values in cervical cancer by multiple databases. By analysis, we obtained 83 co-expressed differential genes from the GEO database (GSE63514, GSE67522 and GSE39001). GO and KEGG enrichment analysis showed that these 83 co-expressed it mainly involved differential genes in DNA replication, cell division, cell cycle, etc.. The PPI network was constructed and top 10 genes with protein-protein interaction were selected. Then, we validated ten genes using some databases such as TCGA, GTEx and oncomine. Survival analysis demonstrated significant differences in CDC45, RFC4, TOP2A. Differential expression analysis showed that these genes were highly expressed in cervical cancer tissues. Furthermore, univariate and multivariate cox regression analysis indicated that CDC45 and clinical stage IV were independent prognostic factors for cervical cancer. In addition, the HPA database validated the protein expression level of CDC45 in cervical cancer. Further studies investigated the relationship between CDC45 and tumor-infiltrating immune cells via CIBERSORT. Finally, gene set enrichment analysis (GSEA) showed CDC45 related genes were mainly enriched in cell cycle, chromosome, catalytic activity acting on DNA, etc. These results suggested CDC45 may be a potential biomarker associated with the prognosis of cervical cancer.

Angiotensinogen and the Modulation of Blood Pressure.

The angiotensin peptides that control blood pressure are released from the non-inhibitory plasma serpin, angiotensinogen, on cleavage of its extended N-terminal tail by the specific aspartyl-protease, renin. Angiotensinogen had previously been assumed to be a passive substrate, but we describe here how recent studies reveal an inherent conformational mechanism that is critical to the cleavage and release of the angiotensin peptides and consequently to the control of blood pressure. A series of crystallographic structures of angiotensinogen and its derivative forms, together with its complexes with renin show in molecular detail how the interaction with renin triggers a profound shift of the amino-terminal tail of angiotensinogen with modulation occurring at several levels. The tail of angiotensinogen is restrained by a labile disulfide bond, with changes in its redox status affecting angiotensin release, as demonstrably so in the hypertensive complication of pregnancy, pre-eclampsia. The shift of the tail also enhances the binding of renin through a tail-in-mouth allosteric mechanism. The N-terminus is now seen to insert into a pocket equivalent to the hormone-binding site on other serpins, with helix H of angiotensinogen unwinding to form key interactions with renin. The findings explain the precise species specificity of the interaction with renin and with variant carbohydrate linkages. Overall, the studies provide new insights into the physiological regulation of angiotensin release, with an ability to respond to local tissue and temperature changes, and with the opening of strategies for the development of novel agents for the treatment of hypertension.

Long non­coding RNA AC245100.4 promotes prostate cancer tumorigenesis via the microRNA­145­5p/RBBP5 axis.

Long non­coding RNAs (lncRNAs) are markedly involved in cancer progression. Thus, identification of these lncRNAs can aid in the treatment of cancer. The present study focused on investigating the overall biological function, mechanism of action and clinical importance of lncRNA AC245100.4 in prostate cancer (PCa). The present study identified that AC245100.4 expression was significantly upregulated in PCa tissues and cell lines. Knockdown of AC245100.4 impaired tumor growth in an animal model. Biological function analysis indicated that AC245100.4 overexpression notably promoted cell proliferation and migration, while knockdown of AC245100.4 suppressed cell proliferation and migration. Mechanism studies focused on the competing endogenous RNA (ceRNA) network of AC245100.4. Bioinformatics predictions indicated that both AC245100.4 and retinoblastoma binding protein 5 (RBBP5) had microRNA (miR) response elements for miR­145­5p. This was further verified using a dual luciferase and RNA immunoprecipitation assays. AC245100.4 could positively regulate RBBP5 expression, but negatively regulated miR­145­5p expression. In addition, AC245100.4 knockdown­mediated inhibitory effects on cell proliferation and migration could be reversed by miR­145­5p silencing. Overall, the present study proposed a novel model in which the AC245100.4/miR­145­5p/RBBP5 ceRNA network induced the development of PCa, providing novel insights for PCa treatment.

Corrigendum: Data Mining and Expression Analysis of Differential lncRNA ADAMTS9-AS1 in Prostate Cancer.

[This corrects the article DOI: 10.3389/fgene.2019.01377.].

LINC00491 as a new molecular marker can promote the proliferation, migration and invasion of colon adenocarcinoma cells.

BACKGROUND: Long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of multiple tumors. However, the roles of lncRNAs during colon adenocarcinoma and cancer progression remain unclear. This study aimed identify new lncRNAs that act as molecular markers for the prevention and diagnosis of colon adenocarcinoma. METHODS: RNA sequencing (RNA-Seq) data associated with colon adenocarcinoma were retrieved from the Cancer Genome Atlas (TCGA). Biological processes in Gene Ontology (Go) and the Kyoto Encyclopedia of Genomes (KEGG) were searched for pathways at the significance level. The expression of LINC00491 and its downstream targets were assessed by real-time PCR, Western blotting and dual-luciferase assays. Biological functions of LINC00491 during cell proliferation, migration and invasion were assessed using CCK-8, colony formation assays, wound healing, and transwell invasion assays in colon adenocarcinoma HT-29 and HCT116 cells. RESULTS: Bioinformatics analysis with the TCGA colon adenocarcinoma dataset showed that LINC00491 was significantly up-regulated in colon adenocarcinoma. Furthermore, we found that LINC00491 positively regulates SERPINE1 expression through sponging miR-145 and promoting the proliferation, migration, and invasion of colon adenocarcinoma cells, thus playing an oncogenic role during colon adenocarcinoma pathogenesis. CONCLUSION: LINC00491 functions as a ceRNA to promote SERPINE1 expression by sponging miR-145. LINC00491 serves as a therapeutic target and prognostic biomarker in colon adenocarcinoma.

miR-124-3p availability is antagonized by LncRNA-MALAT1 for Slug-induced tumor metastasis in hepatocellular carcinoma.

BACKGROUND: As an oncogene, long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) can promote tumor metastasis. Hyperexpression of MALAT1 has been observed in many malignant tumors, including hepatocellular carcinoma (HCC). However, the role and mechanism of MALAT1 in HCC remain unclear. METHODS: Thirty human HCC and paracancerous tissue specimens were collected, and the human hepatoma cell lines Huh7 and HepG2 were cultured according to standard methods. MALAT1 and Snail family zinc finger (Slug) expression were measured by real-time PCR, immunohistochemistry, and western blotting. Luciferase reporter assay and RNA immunoprecipitation (RIP) assay verified the direct interaction between miR-124-3p and Slug(SNAI2) or MALAT1. Wound healing and transwell assays were performed to examine invasion and migration, and a subcutaneous tumor model was established to measure tumor progression in vivo. RESULTS: MALAT1 expression was upregulated in HCC tissues and positively correlated with Slug expression. MALAT1 and miR-124-3p bind directly and reversibly to each other. MALAT1 silencing inhibited cell migration and invasion. miR-124-3p inhibited HCC metastasis by targeting Slug. CONCLUSIONS: MALAT1 regulates Slug through miR-124-3p, affecting HCC cell metastasis. Thus, the MALAT1/miR-124-3p/Slug axis plays an important role in HCC.

Identification of competitive endogenous RNAs network in breast cancer.

BACKGROUND: MiRNAs can regulate gene expression directly or indirectly, and long noncoding RNAs as competing endogenous RNA (ceRNAs) can bind to miRNAs competitively and affect mRNA expression. The ceRNA network is still unclear in breast cancer. In this study, a ceRNA network was constructed, and new treatment and prognosis targets and biomarkers for breast cancer were explored. METHODS: A total of 1 096 cancer tissues and 112 adjacent normal tissues to cancer from the TCGA database were used to screen out significant differentially expressed mRNAs (DEMs), lncRNAs (DELs), and miRNAs (DEMis) to construct a ceRNA network. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were used to predict potential functions. Survival analysis was performed to predict which functions were significant for prognosis. RESULTS: From the analysis, 2 139 DEMs, 1 059 DELs, and 84 DEMis were obtained. Targeting predictions for DEMis-DELs and DEMis-DEMs can yield 26 DEMs, 90 DELs, and 18 DEMis. We performed GO enrichment analysis, and the results showed that the upregulated DEMs were involved in nucleosomes, extracellular regions, and nucleosome assembly, while the downregulated DEMs were mainly involved in Z disk, muscle contraction, and structural constituents of muscle. KEGG pathway analysis was performed on all DEMs, and the pathways were enriched in retinol metabolism, steroid hormone biosynthesis, and tyrosine metabolism. Through survival analysis of the ceRNA network, we identified four DEMs, two DELs, and two DEMis that were significant for poor prognosis. CONCLUSIONS: This study suggested that constructing a ceRNA network and performing survival analysis on the network could screen out new significant treatment and prognosis targets and biomarkers.

Data Mining and Expression Analysis of Differential lncRNA ADAMTS9-AS1 in Prostate Cancer.

Long noncoding RNAs (lncRNAs) play important roles in the regulation of gene expression by acting as competing endogenous RNAs (ceRNAs). However, the roles of lncRNA-associated ceRNAs in oncogenesis are not fully understood. The present study aims to determine whether a ceRNA network can serve as a prognostic marker in human prostate cancer (PCa). In order to identify a ceRNA network and the key lncRNAs in PCa, we constructed a differentially expressed lncRNAs (DELs)-differentially expressed miRNAs (DEMis)-differentially expressed mRNAs (DEMs) regulatory network based on the ceRNA theory using data from the Cancer Genome Atlas (TCGA). We found that the DELs-DEMis-DEMs network was composed of 27 DELs nodes, seven DEMis nodes, and three DEMs nodes. The 27 DELs were further analyzed with several public databases to provide meaningful information for understanding the functional roles of lncRNAs in regulatory networks in PCa. We selected ADAMTS9-AS1 to determine its role in PCa and found that ADAMTS9-AS1 significantly influences tumor cell growth and proliferation, suggesting that it plays a tumor suppressive role. In addition, ADAMTS9-AS1 functioned as ceRNA, effectively becoming a sponge for hsa-mir-96 and modulating the expression of PRDM16. These results suggest that ceRNAs could accelerate biomarker discovery and therapeutic strategies for PCa.