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.

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.

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.

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.