New insight into the mechanism of biofouling-resistant thiazole-linked covalent organic frameworks for selective uranium capture from seawater.

The extraction of uranium from seawater is crucial for the sustainable production of nuclear fuel. Traditional amidoxime-functionalized adsorbents suffer from competitive adsorption of vanadium ion and biofouling. These challenges motivate the development of novel adsorbents for selective uranium extraction from seawater. Herein, four kinds of thiazole-linked covalent organic frameworks (COFs) were investigated to harvest uranium from seawater. The selectivity and anti-biofouling performance were systematically investigated through the molecular dynamics (MD) simulations. Driven by the pore size sieving effect and electrostatic interaction, the Ca2UO2(CO3)3 complex and vanadate anions were selectively separated by different COFs in special areas. On one hand, benefits from the small steric partition factor, the Ca2UO2(CO3)3 complex can stick on the surface of COFs. On the other hand, the dispersive negatively and positively charged areas of studied COFs work as potential binding sites for the Ca2UO2(CO3)3 complex and vanadate anions, respectively. Moreover, an analysis of pulling force and desorption time between uranium and vanadium ions further confirmed the selectivity of various thiazole-linked COFs. The anti-biofouling property was comparatively investigated by dynamic trajectory and solvent accessible surface area. Our outcomes illustrate that the hydroxyl and zwitterionic groups in the thiazole-linked COFs endow their strong surface hydrations to resist marine biofouling. In particular, the TpBdsaPa is identified as a promising candidate due to charge dispersed zwitterionic group as well as remarkable anti-biofouling ability. The present study sheds an atomic-level understanding of the thiazole-linked COFs for selective uranium uptaking from seawater, which will provide aid to design novel adsorbent with highly selective uranium extraction capacity and strong anti-biofouling property.

Bioinformatics Analysis of GFAP as a Potential Key Regulator in Different Immune Phenotypes of Prostate Cancer.

Tumor immune escape plays an essential role in both cancer progression and immunotherapy responses. For prostate cancer (PC), however, the molecular mechanisms that drive its different immune phenotypes have yet to be fully elucidated. Patient gene expression data were analyzed from The Cancer Genome Atlas-prostate adenocarcinoma (TCGA-PRAD) and the International Cancer Genome Consortium (ICGC) databases. We used a Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT) analysis and an unsupervised clustering analysis to identify patient subgroups with distinct immune phenotypes. These distinct phenotypes were then explored for associations for differentially expressed genes (DEGs) and both epigenetic and genetic landscapes. Finally, we used a protein-protein interaction analysis to identify key hub genes. We identified two patient subgroups with independent immune phenotypes associated with the expression of Programmed death-ligand 1 (PD-L1). Patient samples in Cluster 1 (C1) had higher scores for immune-cell subsets compared to Cluster 2 (C2), and C2 samples had higher specific somatic mutations, MHC mutations, and genomic copy number variations compared to C1. We also found additional cluster phenotype differences for DNA methylation, microRNA (miRNA) expression, and long noncoding RNA (lncRNA) expression. Furthermore, we established a 4-gene model to distinguish between clusters by integrating analyses for DEGs, lncRNAs, miRNAs, and methylation. Notably, we found that glial fibrillary acidic protein (GFAP) might serve as a key hub gene within the genetic and epigenetic regulatory networks. These results improve our understanding of the molecular mechanisms underlying tumor immune phenotypes that are associated with tumor immune escape. In addition, GFAP may be a potential biomarker for both PC diagnosis and prognosis.

STAT3-Induced Upregulation of lncRNA CASC9 Promotes the Progression of Bladder Cancer by Interacting with EZH2 and Affecting the Expression of PTEN.

OBJECTIVE: Long non-coding RNA (lncRNA) cancer susceptibility candidate 9 (CASC9) has been reported to play a vital role in tumorigenesis. This study explored the biological role of CASC9 and its regulation mechanism in bladder cancer (BC). METHODS: Gene expression was evaluated using quantitative reverse transcription polymerase chain reaction and Western blot. The functional role of CASC9 in BC was studied using Cell Counting Kit-8, colony formation assay, scratch wound healing assay, transwell invasion assay, and xenograft tumor assay. In addition, the mechanism of CASC9 function in BC was determined using RNA immunoprecipitation assay and chromatin immunoprecipitation assay. RESULTS: CASC9 was upregulated in BC tissues and cell lines, and correlated with the staging and metastasis in BC. Knockdown of CASC9 inhibited the proliferation, migration, and invasion of BC cells. Similarly, silencing of CASC9 inhibited tumor growth in vivo. Signal transducer and activator of transcription 3 (STAT3) was upregulated in BC tissues and cell lines, and positively correlated with CASC9 in BC tissues. Moreover, CASC9 was shown to be regulated by STAT3 in BC cells. Furthermore, CASC9 regulated phosphatase and tensin homolog (PTEN) expression by interacting with enhancer of zeste homolog 2 (EZH2). More significantly, CASC9 silencing-mediated inhibition of BC progression was partly reversed by EZH2 overexpression or PTEN inhibition. CONCLUSION: Upregulation of CASC9 induced by STAT3 promoted the progression of BC by interacting with EZH2 and affecting the expression of PTEN, representing a novel regulatory mechanism for BC progression.

Identification of differentially expressed microRNAs during preadipocyte differentiation in Chinese crested duck.

MicroRNAs (miRNAs) are considered key players in the regulation of a broad range of biological processes. Specifically, miRNAs have been reported to play an important role in the process of adipogenesis. In this study, we constructed a model of adipogenesis by isolating preadipocytes (WCC) derived from adipose tissue and preadipocytes after 72 h differentiation (WCT) in vitro. Deep sequencing of miRNAs expressed in WCT and WCC cells was conducted; we identified 105 differentially expressed miRNA candidates (fifty up-regulated and fifty-five down-regulated). Among them, twelve were novel miRNAs, and ninety-three were previously known miRNAs. Furthermore, seven miRNAs were selected for expression confirmation by reverse transcription quantitative PCR (RT-qPCR); the results showed that the differential expression of miRNAs between the two groups was consistent with our sequencing results. Of them, miR-223, miR-184-3p, and miR-10b-5 showed a strong correlation to adipogenesis. Using target prediction, we predicted that the 105 differentially expressed miRNAs targeted 4155 unique mRNAs. The prediction of targets of differentially expressed miRNAs revealed that the miRNAs participated in the regulation of multiple adipogenesis-related signalling pathways, including the peroxisome proliferator-activated receptor (PPAR) signalling pathway, insulin signalling pathway, fatty acid biosynthesis, and fatty acid degradation. Overall, our findings provide a background for further research into miRNAs and lay a foundation for the prediction and analysis of miRNAs related to adipogenesis.