YTHDF2 promotes arsenic-induced malignant phenotypes by degrading PIDD1 mRNA in human keratinocytes.

Arsenic is a widespread environmental carcinogen, and its carcinogenic mechanism has been the focus of toxicology. N-methyladenosine (mA) binding protein YTH domain family protein 2 (YTHDF2) performs various biological functions by degrading mA-modified mRNAs. However, the mA-modified target mRNA of YTHDF2 in regulating arsenic carcinogenesis remains largely unknown.

YTHDF2 phase separation promotes arsenic-induced keratinocyte transformation in a poly-mA-dependent manner by inhibiting translational initiation of the key tumor suppressor PTEN.

The phase separation of N-methyladenosine (mA) binding protein YTHDF2 plays a vital role in arsenic-induced skin damage, and YTHDF2 can bind to mA-methylated mRNA of tumor suppressor PTEN. However, whether and how YTHDF2 phase separation regulates PTEN involved in arsenic-induced malignant transformation of keratinocytes remains blank. Here, we established arsenite-induced transformation models with stable expression of wild-type YTHDF2 or mutant YTHDF2 protein in vitro and in vivo.

Bacterial contamination in the different parts of household air conditioners: a comprehensive evaluation from Chengdu, Southwest China.

Introduction: Air flow driven by air-conditioner has a significant impact on the indoor environment, however, the bacterial contamination conditions in the different parts of air-conditioners have not been fully elucidated.

Methods: In this study, we assessed the bacterial pollution in the four parts, including air outlet, filter net, cooling fin and water sink, of ten household air-conditioners quantitatively and qualitatively from Chengdu, southwestern China.

Results: The microbial cultivation results showed the large total bacterial counts of 5042.

Bacterial Contamination in the Different Parts of Household Washing Machine: New Insights from Chengdu, Western China.

The moist and warm environment in the household washing machine provides ideal living conditions for the growth and survival of various microorganisms. However, the biodiversity of bacterial community in the different parts of washing machine from Chinese households has not been clarified. In this study, we assessed the bacterial communities in sealing strip, detergent drawer, inner drum, water filter and greywater of ten domestic washing machines quantitatively and qualitatively in Chengdu, southwestern China.

Spatial-temporal distribution and source analysis of atmospheric particulate-bound cadmium from 1998 to 2021 in China.

Cadmium (Cd) is one of the most serious atmospheric heavy metal pollutants in China. PM, PM, and total suspended particle (TSP) are all important media for population Cd exposure. However, no studies so far have systematically explored the spatial and temporal distribution of atmospheric Cd bound to all these media in China, and the specific industrial sectors that contribute to the airborne Cd level are still unclear at present.

N-methyladenosine promotes aberrant redox homeostasis required for arsenic carcinogenesis by controlling the adaptation of key antioxidant enzymes.

N-methyladenosine (mA), a high-profile RNA epigenetic modification, responds to oxidative stress and temporal-specifically mediates arsenic carcinogenesis. However, how mA affects aberrant redox homeostasis required for arsenic carcinogenesis is poorly understood. Here, we established arsenic-carcinogenic models of different stages, including As-treated, As-transformed, and As-tumorigenic cell models.

Long-term exposure to cadmium disrupts neurodevelopment in mature cerebral organoids.

Cadmium (Cd) is a pervasive environmental pollutant. Increasing evidence suggests that Cd exposure during pregnancy can induce adverse neurodevelopmental outcomes. However, due to the limitations of neural cell and animal models, it is challenging to study the developmental neurotoxicity and underlying toxicity mechanism of long-term exposure to environmental pollutants during human brain development.

Oxidative Stress Induced by Arsenite is Involved in YTHDF2 Phase Separation.

YTH N-methyladenosine RNA binding protein 2 (YTHDF2) undergoes phase separation in response to the stimulation of high concentration of arsenite, suggesting that oxidative stress, the major mechanism of arsenite toxicity, may play a role in YTHDF2 phase separation. However, whether arsenite-induced oxidative stress is involved in phase separation of YTHDF2 has yet to be established. To explore the effect of arsenite-induced oxidative stress on YTHDF2 phase separation, the levels of oxidative stress, YTHDF2 phase separation, and N-methyladenosine (mA) in human keratinocytes were detected after exposure to various concentrations of sodium arsenite (0-500 µM; 1 h) and antioxidant N-acetylcysteine (0-10 mM; 2 h).

N-methyladenosine upregulates ribosome biogenesis in environmental carcinogenesis.

Many trace metal pollutants in surface water, the atmosphere, and soil are carcinogenic, and ribosome biogenesis plays an important role in the carcinogenicity of heavy metals. However, the contradiction between upregulated ribosome biogenesis and decreased ribosomal DNA copy number in environmental carcinogenesis is not fully understood. Here, from a perspective of the most predominant and abundant RNA epigenetic modification, N-methyladenosine (mA), we explored the reason behind this contradiction at the post-transcriptional level using arsenite-induced skin carcinogenesis models both in vitro and in vivo.

N-methyladenosine plays a dual role in arsenic carcinogenesis by temporal-specific control of core target AKT1.

High-profile RNA epigenetic modification N-methyladenosine (mA), as a double-edged sword for cancer, can either promote or inhibit arsenic-induced skin carcinogenesis. However, the core mA-target gene determining the duality of mA and the regulatory mechanism of mA on the core gene are still poorly understood. Based on mA microarray detection, integrated multi-omics analysis, and further experiments in vitro and in vivo, we explored the molecular basis for the dual role of mA in cancer induced by environmental pollutants using models in different stages of arsenic carcinogenesis, including As-treated, As-transformed, and As-tumorigenic cell models.

[Mechanism of Triclosan in the Treatment of Nonalcoholic Fatty Liver Disease Based on Network Pharmacology].

Objective To explore the potential targets of triclosan in the treatment of nonalcoholic fatty liver disease(NAFLD) and to provide new clues for the future research on the application of triclosan. Methods The targets of triclosan and NAFLD were obtained via network pharmacology.The protein-protein interaction network was constructed with the common targets shared by triclosan and NAFLD.

Triclosan targeting of gut microbiome ameliorates hepatic steatosis in high fat diet-fed mice.

Antibiotic use provides a promising strategy for the treatment of non-alcoholic fatty liver disease (NAFLD) by regulating the gut microbiota composition. Triclosan, a widely used antibiotic, may improve gut microbiome dysbiosis associated with NAFLD through the suppression of pathogenic gram-negative bacteria. However, the effects of triclosan on gut microbiota and hepatic steatosis and have not been explored in NAFLD mouse model.

Alveolar macrophage-derived progranulin mediated pro-inflammatory Il-6 expression via regulating Creb1 in silicosis model.

Progranulin (PGRN) is a secreted factor involved in inflammatory diseases. However, the function of PGRN in silica-induced lung inflammation has not been elucidated. In this study, we demonstrated that PGRN in serum and lung tissues was markedly increased in silicosis mouse model.

[Comparative Analysis of Direct Drinking Water and the Relevant Sanitation Standards in China].

Along with the economic and technological development and growing demand for high-quality drinking water, direct drinking water has gained general popularity in China. However, no authoritative policy has been issued, giving a clear definition of direct drinking water and existing standards and regulations concerning direct drinking water are not definitive in nature. Existing water quality parameters are not well supported and sometimes even contradict each other.

Triclosan down-regulates fatty acid synthase through microRNAs in HepG2 cells.

Triclosan is a promising candidate of fatty acid synthase (FASN) inhibitor by blocking FASN activity, but its effect on FASN expression and the underling epigenetic mechanism remain elusive. In this study, the effect of triclosan on FASN mRNA and protein expressions in human HepG2 cells and the regulatory role of microRNAs (miRNAs) in the downregulation of FASN induced by triclosan were explored through experiments and bioinformatics analysis. The results showed that triclosan not only directly inhibited FASN activity, but also significantly decreased FASN mRNA and protein levels in human liver HepG2 cells.

China's drinking water sanitation from 2007 to 2018: A systematic review.

Regular monitoring of drinking water in China is carried out by the Centers for Disease Control and Prevention at all levels and some articles were published for the public to understand the status of drinking water. However, these published articles were limited to small areas and reported almost exclusively in Chinese. In order to give the public a comprehensive understanding of the situation of drinking water sanitation in China and provide specific directions for ensuring drinking water safety in the future, we review the sanitation status of drinking water in different regions of China from 2007 to 2018, the changes over time and the factors affecting drinking water quality by means of systematic review for the first time.

Fat mass and obesity-associated protein regulates lipogenesis via m A modification in fatty acid synthase mRNA.

As the first identified N -methyladenosine (m A) demethylase, fat mass and obesity-associated (FTO) protein is associated with fatty acid synthase (FASN) and lipid accumulation. However, little is known about the regulatory role of FTO in the expression of FASN and de novo lipogenesis through m A modification. In this study, we used FTO small interfering RNA to explore the effects of FTO knockdown on hepatic lipogenesis and its underlying epigenetic mechanism in HepG2 cells.

Linc-ROR promotes arsenite-transformed keratinocyte proliferation by inhibiting P53 activity.

Linc-ROR is an oncogenic long non-coding RNA over-expressed in many kinds of cancer that promotes cancer cell proliferation. Arsenite is a determined carcinogen that increases the risk of skin cancer, but the carcinogenic mechanism of arsenite remains unclear. To explore whether and how linc-ROR plays a role in arsenite-induced carcinogenesis of skin cancer, we established arsenite-transformed keratinocyte HaCaT cells by exposing them to 1 μM arsenite for 50 passages.

Arsenite Increases Linc-ROR in Human Bronchial Epithelial Cells that Can Be Inhibited by Antioxidant Factors.

Oxidative stress is the main mechanism of arsenite toxicity. Long intergenic non-coding RNA regulator of reprogramming is a newly found stress-response long non-coding RNA that is activated in various stress conditions. However, whether long intergenic non-coding RNA, regulator of reprogramming (linc-ROR) is involved in arsenite-induced oxidative stress has not been explored.

Long non-coding RNA ROR confers arsenic trioxide resistance to HepG2 cells by inhibiting p53 expression.

Arsenic trioxide is an effective drug in the treatment of hematologic malignancies, but it has no obvious therapeutic effect on liver cancer. Long non-coding RNA ROR is a newly found long-noncoding RNA that has been reported to get involved in the regulation of chemo-resistance in multiple cancers. However, whether and how long non-coding RNA ROR gets involved in the resistance to arsenic trioxide in liver cancer has not been explored.

N-methyladenosine mediates arsenite-induced human keratinocyte transformation by suppressing p53 activation.

N-methyladenosine (mA), the most abundant and reversible RNA modification, plays critical a role in tumorigenesis. However, whether mA can regulate p53, a leading antitumor protein remains poorly understood. In this study, we explored the regulatory role of mA on p53 activation using an arsenite-transformed keratinocyte model, the HaCaT-T cell line.

Genotoxicity assessment of triclocarban by comet and micronucleus assays and Ames test.

The widespread usage and ubiquitous distribution of triclocarban (3,4,4'-trichlorocarbanilide, TCC) have raised public concerns about its health effects. At present, there is little information about the genotoxicity of TCC. In this study, we used a battery of genotoxicity testing methods including salmonella reverse mutation test (Ames test), comet assay and micronucleus assay to detect the effects of TCC on gene mutation, DNA breakage, and chromosome damage.

Inhibition of base excision repair by natamycin suppresses prostate cancer cell proliferation.

Prostate cancer (PCa) progression is characterized by increased expression and transcriptional activity of the androgen receptor (AR). In the advanced stages of prostate cancer, AR significantly upregulates the expression of genes involved in DNA repair. Upregulation of expression for base excision repair (BER) related genes is associated with poor patient survival.

Preoperative serum ferritin is an independent prognostic factor for liver cancer after hepatectomy.

Background And Aims: Serum ferritin (SF) may have a close relationship with the tumor. But no study has investigated the prognostic value of SF in hepatocellular carcinoma (HCC) patients receiving curative resection yet. Aim of this study is to explore the role of preoperative SF in survival outcomes of such patients.

Evaluation of DNA and chromosomal damage in two human HaCaT and L02 cells treated with varying triclosan concentrations.

Triclosan has been used in a large number of consumer products and concerns have been raised over regarding potential genotoxicity. However, the genotoxicity of triclosan has not been assessed in normal human cells. The aim of this study was to examine the potential genotoxicity using the comet assay and micronucleus (MN) test to detect DNA damage and chromosomal breakage attributed to triclosan in human keratinocyte HaCaT and hepatic L02 cells.