Environmental contamination and risks of organic UV filters: Source, discharge, analytical methods and implications for ecological and human health.

Organic Ultraviolet Filters (OUVFs), commonly used in sunscreens, cosmetics and industrial products to prevent ultraviolet radiation damage, are increasingly detected in the environment due to their widespread use and persistence. This has raised concerns over their toxicity and environmental impact, leading to the classification of OUVF 2-(2H-Benzotriazol-2-yl)-4,6-ditertpentylphenol (UV-328) as a persistent organic pollutant under the Stockholm Convention in 2023. In this review, current knowledge on the usage, discharge and environmental contamination of OUVFs is briefly discussed. The available analytical methodologies are also reviewed, especially for the extraction and detection of OUVFs in different matrix samples. Finally, the reported levels of OUVFs pollution in surface water, drinking water, aquatic organisms and human urine worldwide are discussed, along with their potential implications for ecological and human health. In general, typical OUVFs ethylhexyl methoxy cinnamate (EHMC) and Octocrylene (OC) have been shown to pose a significant potential risks in the surface waters of multiple countries such as Australia, China, Japan, the United States. Furthermore, while the OUVFs exposure concentrations in drinking water are generally low (below detection limit to 450 ng/L), prolonged exposure may still present potential health risks for humans.

Ferroptosis signaling promotes the release of misfolded proteins via exosomes to rescue ER stress in hepatocellular carcinoma.

Dysfunction of the ubiquitin‒proteasome system can induce sustained endoplasmic reticulum stress (ERS) and subsequent cell death. However, malignant cells have evolved multiple mechanisms to evade sustained ERS. Therefore, identification of the mechanisms through which tumor cells develop resistance to ERS is important for the therapeutic exploitation of these cells for drug-resistant tumors. Herein, we found that proteasome inhibitors could induce ERS, activate ferroptosis signaling, and thereby induce the adaptive tolerance of tumor cells to ERS. Mechanistically, the activation of ferroptosis signaling was found to promote the formation and secretion of exosomes containing misfolded and unfolded proteins, which resulted in rescuing ERS and promoting tumor cell survival. The inhibition of ferroptosis signaling synergized with bortezomib, a clinically used proteasome inhibitor, to suppress the viability of hepatocellular carcinoma cells in vitro and in vivo. The present findings reveal that ERS resistance can be driven by an ERS-ferroptosis signaling-exosome pathway and have important clinical implications for intracellular signaling, ER homeostasis and drug-resistant cancer therapy.

miR-21 targets the tumor suppressor RhoB and regulates proliferation, invasion and apoptosis in colorectal cancer cells.

It has become increasingly clear that microRNAs play an important role in many human diseases including cancer. Here, we show that expression of miR-21 in HEK293 and several colorectal cancer cells was found inversely correlated with ras homolog gene family, member B (RhoB) expression. miR-21 expression significantly suppressed RhoB 3' UTR luciferase-reporter activity, but the inhibitory effect was lost when the putative target sites were mutated. Exogenous miR-21 over-expression mimicked the effect of RhoB knockdown in promoting proliferation and invasion and inhibiting apoptosis, whereas anti-miR-21 or RhoB expression yielded opposite effects, in colorectal cancer cells. These results suggest that miR-21 is a regulator of RhoB expression and RhoB could be a useful target in exploring the potential therapeutic benefits of miR-21 mediated tumor cell behaviors in colorectal cancer.