Bio-availability of potential trace elements in urban dust, soil, and plants in arid northwest China.

Potential trace elements pollution in cities poses a threat to the environment and human health. Bio-availability affects toxicity levels of potential trace elementss on organisms. This study focused on exploring the relationship between soil, plant, and atmospheric dust pollution in Urumqi, a typical city in western China. It aims to help reduce pollution and protect residents' health. The following conclusions were drawn: 1) potential trace elementss like Cr, Pb, As, and Ni are more prevalent in atmospheric dust and soil than in plants. Chromium was in the first group, Cadmium and Mercury were in the second, and Plumb, Arsenic, and Nickel were in the third. Atmospheric dust and soil exhibit a significantly higher heavy metal content than plants. For example, The atmospheric dust summary Chromium content was up to 88 mg/kg. 2) Soil, atmospheric dust, and plants have the highest amount of residual form. Residual form had the highest percentage average of 53.3%, whereas Organic matter bound form had the lowest percentage of just 7.7%. The plants contained less residual heavy metal than the soil and atmospheric dust. 3) The correlation coefficient between the carbonated form content of Cd of soil and atmospheric dust is 0.95, which is closely related. Other potential trace elements show similar correlations in their bio-available contents in soil, plants, and atmospheric dust. This study suggests that in urban area, the focus should be on converting potential trace elements into residual form instead of increasing plants' absorption of potential trace elements.

The current research in China primarily examines heavy metal pollution in the atmosphere, soil, and plants individually. Although there is significant international research on heavy metal bio-availability in the environment, few studies have focused on the presence of heavy metals in soil, vegetation, and atmospheric dust.Therefore, this study focused on Urumqi, the capital of Xinjiang, a typical oasis city in the arid region. To understand the bio-availability and morphological characteristics of heavy metals (Cd, Pb, Hg, Cr, As, Ni) in the soil-plant-atmosphere of its urban expressway.This study aims to establish a theoretical basis for understanding the pollution hazards caused by heavy metals in oasis cities. It will have practical significance in maintaining urban ecology, promoting sustainable development, and safeguarding citizens' health.

Evaluating the capacity of heavy metal pollution enrichment in green vegetation in the industrial zone, Northwest China.

It focused on heavy metal pollution of green vegetation in Tuokexun County, Xinjiang Northwest China's suburban industrial area, using inductively coupled plasma emission spectrometer to analyze the samples for Mn, Ni, Zn, Cd, Hg, Pb, As, Cu, and Cr contents. The soil's heavy metal content in the study area indicated a minor level of pollution overall (P = 1.77), with the most severe contamination being Hg, which is more likely to be caused by human activities. Heavy metal elements in trees have the most stable composition in comparison to grass and shrubs, with varying concentrations across different vegetation. The concentrations of Mn, Cd and Hg were highest in the Haloxylon ammodendron, Ni in Morus alba, Pb, As and Cu in Nitraria tangutorums, and Cr in Phragmites australis. Heavy metal restoration is most effectively performed by shrubs, and there are disparities in heavy metal enrichment among various vegetation. No significant difference was found in heavy metal enrichment between the aboveground and underground parts of vegetation. Based on the average of the membership function, Tamarix exhibits the strongest ability to enrich heavy metals, while Nitraria tangutorum comes in second, and Cynanchum chinense R.Br. is the least effective among all plant species. Morus alba is recommended as the primary planting species in the area. Nitraria tangutorum and Haloxylon ammodendron have good potential for Cd and As restoration and can be used as supporting vegetation.

MicroRNA-506 has a suppressive effect on the tumorigenesis of nonsmall-cell lung cancer by regulating tubby-like protein 3.

MicroRNA-506 (miR-506), a miRNA, has been proven to act as a tumor suppressor gene in nonsmall-cell lung cancer (NSCLC); Tubby-like protein 3 (TULP3) is a potential target gene of miR-506. This study investigates whether miR-506 can prevent NSCLC progression by mediating TULP3. In vivo and in vitro experiments were performed to explore the function and potential regulatory relationship of miR-506 and TULP3 in NSCLC. Our results revealed that miR-506 is high expression in NSCLC cell lines, and the overexpression of miR-506 could inhibit cell viability and enhance cell apoptosis in H1299 and A549 cells. Pro-apoptotic related protein (cytochrome C, Bax, and cleaved caspase-9) expression increased while anti-apoptotic related protein (BCL-2 and BCL-XL) expression decreased after miR-506 was overexpression. Meanwhile, the overexpression of miR-506 could notably downregulate TULP3. Additionally, silence of TULP3 inhibited cell viability and promoted cell apoptosis. At the same time, pro-apoptotic related protein expression was promoted while anti-apoptotic related protein expression was inhibited. Furthermore, TULP3 overexpression could markedly reverse the inhibitory effect of miR-506 on the proliferation and induction of mitochondrial apoptosis in H1299 and A549 cells. In vivo tumor formation experiments also exhibited consistent results indicating that the functions of TULP3 might be correlated with the promotion of tumorigenesis. In conclusion, we firstly found that miR-506 can be involved in the processes of NSCLC and exert a suppressive effect on tumorigenesis by regulating TULP3 expression.

Gallic acid from Terminalia chebula inhibited the growth of esophageal carcinoma cells by suppressing the Hippo signal pathway.

OBJECTIVES: To explore the molecular mechanism of gallic acid (GA) from Terminalia chebula in suppressing the growth of esophageal carcinoma (EC). MATERIALS AND METHODS: Human EC cells (EC9706 and KYSE450) were treated with different concentrations of GA (10, 20, and 40 µg/ml), which were subjected to 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, plate clone formation assay, Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining, and Western blotting. EC mice were divided into Model, 0.3% GA, and 1% GA groups to observe the tumor volume and the expressions of YAP, TAZ, Ki-67, and Caspase-3 in tumor tissues. RESULTS: GA decreased cell viability and colony formation of EC9706 and KYSE450 cells, which was more obvious as the concentration increased. In addition, GA promoted cell apoptosis in a concentration-dependent manner with the up-regulation of pro-apoptotic proteins (Bax, cleaved caspase-3, and cleaved caspase-9) and nuclear YAP/TAZ, as well as the down-regulation of anti-apoptotic protein Bcl-2 and the levels of p-YAP and p-TAZ. Moreover, GA decreased the growth of xenograft tumor in vivo, with the reduction in the tumor volume and the reduction of YAP and TAZ expressions in the tumor tissues. In addition, Ki-67 expression in GA groups was lower than those in the Model group, with the increase in caspase-3 expression in the tumor tissues. Changes aforementioned were obviously shown in the 0.3% GA group. CONCLUSION: GA blocked the activity of the Hippo pathway to suppress cell proliferation of EC and facilitate cell apoptosis, which is expected to be a novel strategy for treatment of EC.

Promising targets and drugs in rheumatoid arthritis: a module-based and cumulatively scoring approach.

AIMS: Rheumatoid arthritis (RA) is a systematic autoimmune disorder, characterized by synovial inflammation, bone and cartilage destruction, and disease involvement in multiple organs. Although numerous drugs are employed in RA treatment, some respond little and suffer from severe side effects. This study aimed to screen the candidate therapeutic targets and promising drugs in a novel method. METHODS: We developed a module-based and cumulatively scoring approach that is a deeper-layer application of weighted gene co-expression network (WGCNA) and connectivity map (CMap) based on the high-throughput datasets. RESULTS: Four noteworthy RA-related modules were identified, revealing the immune- and infection-related biological processes and pathways involved in RA. HLA-DMA, HLA-DMB, HLA-DPA1, HLA-DPB1, HLA-DQB1, HLA-DRA, HLA-DRB1, BLNK, BTK, CD3D, CD4, IL2RG, INPP5D, LCK, PTPRC, RAC2, SYK, and VAV1 were recognized as the key hub genes with high connectivity in gene regulation networks and gene pathway networks. Moreover, the long noncoding RNAs (lncRNAs) in the RA-related modules, such as FAM30A and NEAT1, were identified as the indispensable interactors with the hub genes. Finally, candidate drugs were screened by developing a cumulatively scoring approach based on the selected modules. Niclosamide and the other compounds of T-type calcium channel blocker, IKK inhibitor, and PKC activator, HIF activator, and proteasome inhibitor, which harbour the similar gene signature with niclosamide, were promising drugs with high specificity and broad coverage for the RA-related modules. CONCLUSION: This study provides not only the promising targets and drugs for RA but also a novel methodological insight into the target and drug screening.Cite this article: Bone Joint Res 2020;9(8):501-514.

Identification of hub genes in colon cancer via bioinformatics analysis.

OBJECTIVES: This study aimed to investigate hub genes and their prognostic value in colon cancer via bioinformatics analysis. METHODS: Differentially expressed genes (DEGs) of expression profiles (GSE33113, GSE20916, and GSE37364) obtained from Gene Expression Omnibus (GEO) were identified using the GEO2R tool and Venn diagram software. Function and pathway enrichment analyses were performed, and a protein-protein interaction (PPI) network was constructed. Hub genes were verified based on The Cancer Genome Atlas (TCGA) and Human Protein Atlas (HPA) databases. RESULTS: We identified 207 DEGs, 62 upregulated and 145 downregulated genes, enriched in Gene Ontology terms "organic anion transport," "extracellular matrix," and "receptor ligand activity", and in the Kyoto Encyclopedia of Genes and Genomes pathway "cytokine-cytokine receptor interaction." The PPI network was constructed and nine hub genes were selected by survival analysis and expression validation. We verified these genes in the TCGA database and selected three potential predictors (ZG16, TIMP1, and BGN) that met the independent predictive criteria. TIMP1 and BGN were upregulated in patients with a high cancer risk, whereas ZG16 was downregulated. The immunostaining results from HPA supported these findings. CONCLUSION: This study indicates that these hub genes may be promising prognostic indicators or therapeutic targets for colon cancer.

The Cancer Genome Atlas (TCGA) based m6A methylation-related genes predict prognosis in hepatocellular carcinoma.

The current study aims to investigate the significance of N6-methyladenosine (m6A) methylation-related genes in the clinical prognosis of hepatocellular carcinoma (HCC) using bioinformatics analyses based on The Cancer Genome Atlas (TCGA) database. Transcriptome data and corresponding clinical data on m6A methylation-related genes (including 15 genes) were obtained from TCGA database. Differential expression of 15 genes was identified. Survival curves of subgroups based on m6A methylation-related gene expression levels were plotted. We selected potential predictive genes and analyzed their prognostic values using bioinformatics methods. Eleven genes (METTL3, YTHDF1, YTHDF2, YTHDF3, YTHDC1, YTHDC2, FTO, KIAA1429, HNRNPC, HNRNPA2B1, and RBM15) were found to be overexpressed in HCC. Of these, five genes had worse survival (P < 0.05). There was a significant difference in the survival rate between subgroups with different expression levels of m6A. We selected five potential predictors (METTL3, KIAA1429, ZC3H13, YTHDF1, and YTHDF2) that met the independent predictive value. ZC3H13 was upregulated in patients with high cancer risk, whereas METTL3, KIAA1429, YTHDF1, and YTHDF2 were downregulated. In summary, we found that the expression levels of m6A methylation-related genes were different in patients with HCC and correlated with survival and prognosis. This implies that m6A methylation-related genes may be promising prognostic indicators or therapeutic targets for HCC.

Overexpression of lncRNA TINCR is associated with high-grade, invasive, and recurring tumors, and facilitates proliferation in vitro and in vivo of urothelial carcinoma of the bladder.

OBJECTIVES: The aberrant expression of long noncoding RNAs (lncRNAs) plays roles in cancer development. In this work, we measured the expression of lncRNA terminal differentiation-induced non-coding RNA (TINCR) in urothelial carcinoma of the bladder (UCB), determined its impact on the proliferation of UCB in vitro and in vivo and identified its possible targets. METHODS: The expression levels of genes were measured by Real-Time quantitative Polymerase Chain Reaction (qPCR). Cell proliferation, cell motility, and cell apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, wound healing assay, and ELISA, respectively. Tumor growth in vivo was determined by xenograft formation assay in nude mice. The predicted binding site between TINCR and hsa-miR-125b was confirmed by dual luciferase reporter assay. RESULTS: The expression levels of TINCR were higher in cancerous tissues than that in paired noncancerous tissues of UCB. Higher expression levels of TINCR were positively associated with high-grade, invasive, and recurring tumors. Depletion of TINCR retarded proliferation, decreased motility, increased apoptosis in UCB cells, and markedly reduced tumor growth in xenograft nude mice. The predicted binding site between TINCR and hsa-miR-125b was functional. TINCR downregulated hsa-miR-125b in UCB cells. Hsa-miR-125b mimic reversed the proliferation caused by TINCR up-expression in UCB cells. CONCLUSIONS: Up-regulation of TINCR may act as an unfavorable indicator for the diseasing status of UCB. TINCR facilitates bladder cancer proliferation in vitro and in vivo. Hsa-miR-125b is a target for TINCR in UCB.

Association of TP53 codon 72 genotype polymorphism and environmental factors with esophageal squamous cell carcinoma in the Mongolian population of the Chinese region of Inner Mongolia.

The present study analyzed the association of tumor protein p53 (TP53) Pro72Arg polymorphism with esophageal squamous cell carcinoma (ESCC) in the Mongolian population of Tongliao (Inner Mongolia, China). Restriction fragment length polymorphism-polymerase chain reaction was used to detect the genotype distribution of TP53 Pro72Arg polymorphism in 100 patients with ESCC and 50 healthy controls from the same population. Besides, the correlation between ESCC in Mongolian patients and various factors such as age, sex, cigarette smoking and alcohol consumption was analyzed. χ2 test revealed significant associations between alcohol consumption (P=0.00006) and cigarette smoking (P=0.00076) and ESCC in Mongolian patients. Notably, the Pro72 allele was significantly enriched in patients with ESCC compared with its abundance in the healthy control group, and the genotype of Pro/Arg on p53 codon 72 was confirmed to exhibit a significant correlation with ESCC in Mongolian patients. The present study demonstrated that alcohol drinking and cigarette smoking were risk factors for ESCC in the Mongolian population. Mongolian patients who carry the partocular genotype of Arg/Pro or Pro/Pro on p53 codon 72 may be more likely to develop ESCC. Compared with the p53 codon 72 genotype Arg/Arg, the TP53 Pro72 allele increased the risk of ESCC in Mongolian patients by 1.659-fold.

Genetic 135G/C polymorphism of RAD51 gene and risk of cancer: a meta-analysis of 28,956 cases and 28,372 controls.

The RAD51 gene is essential for the repair of damaged DNA related to tumor development. Although a number of genetic studies have attempted to link the 135G/C polymorphism of RAD51 gene to the risk of cancer, the results were inconclusive. The present study aimed at investigating the pooled association using the more comprehensive meta-analysis. The PubMed, EBSCO, and BIOSIS databases were searched to identify eligible studies which were published in English before March 2014. Data were extracted using standardized methods. The association was assessed by odds ratio (OR) with 95 % confidence interval (CI). Begg's test was used to measure publication bias. Sensitivity analyses were also performed to assess the stability of the results. A total of 45 eligible studies with 28,956 patients and 28,372 controls were included in this meta-analysis. Overall, significant association was detected between 135G/C polymorphism and increased cancer risk (C allele vs. G allele: OR 1.23, 95 % CI 1.18-1.28; CC vs. GG: OR 2.41, 95 % CI 2.12-2.74; CC vs. CG: OR 3.86, 95 % CI 3.41-4.37; recessive model: OR 3.57, 95 % CI 3.19-4.00). In further stratified analysis, significantly elevated cancer risk was observed among Caucasians but not Asians. Subgroup analysis by different cancers also showed their significant associations in breast cancer, hematologic malignances, ovarian cancer, colorectal cancer and endometrial cancer, but not in head and neck cancer. Our results indicated that the RAD51 135G/C polymorphism was a candidate for susceptibility of cancer. The effect of the variants on the expression levels and the possible functional role of the variants in different cancers should be addressed in further studies.