MiR-26a functions as a tumor suppressor in ambient particulate matter-bound metal-triggered lung cancer cell metastasis by targeting LIN28B-IL6-STAT3 axis.

Exposure to ambient particulate matter (PM) has been linked to the increasing incidence and mortality of lung cancer, but the principal toxic components and molecular mechanism remain to be further elucidated. In this study, human lung adenocarcinoma A549 cells were treated with serial concentrations of water-extracted PM10 (WE-PM10) collected from Beijing, China. Our results showed that exposure to 25 and 50 µg/ml of WE-PM10 for 48 h significantly suppressed miR-26a to upregulate lin-28 homolog B (LIN28B), and in turn activated interleukin 6 (IL6) and signal transducer and activator of transcription 3 (STAT3) in A549 cells, subsequently contributing to enhanced epithelial-mesenchymal transition and accelerated migration and invasion. In vivo pulmonary colonization assay further indicated that WE-PM10 enhanced the metastatic ability of A549 cells. In addition, luciferase reporter assay demonstrated that 3' untranslated region of LIN28B was a direct target of miR-26a. Last but not the least, the key toxic contribution of metals in WE-PM10 was confirmed by the finding that removal of metals through chelation significantly rescued WE-PM10-mediated inflammatory, carcinogenic and metastatic responses. Taken together, miR-26a could act as the tumor suppressor in PM10-related lung cancer, and PM10-bound metals promoted lung cancer cell metastasis through downregulation of miR-26a that directly mediated LIN28B expression.

Evaluation of Volatile Organic Compounds and Carbonyl Compounds Present in the Cabins of Newly Produced, Medium- and Large-Size Coaches in China.

An air-conditioned coach is an important form of transportation in modern motorized society; as a result, there is an increasing concern of in-vehicle air pollution. In this study, we aimed to identify and quantify the levels of volatile organic compounds (VOCs) and carbonyl compounds (CCs) in air samples collected from the cabins of newly produced, medium- and large-size coaches. Among the identified VOCs and CCs, toluene, ethylbenzene, xylene, formaldehyde, acetaldehyde, acrolein/acetone, and isovaleraldehyde were relatively abundant in the cabins. Time was found to affect the emissions of the contaminants in the coaches. Except for benzaldehyde, valeraldehyde and benzene, the highest in-vehicle concentrations of VOCs and CCs were observed on the 15th day after coming off the assembly line, and the concentrations exhibited an approximately inverted U-shaped pattern as a function of time. Interestingly, this study also showed that the interior temperature of the coaches significantly affected the VOCs emissions from the interior materials, whereas the levels of CCs were mainly influenced by the relative humidity within the coaches. In China, guidelines and regulations for the in-vehicle air quality assessment of the coaches have not yet been issued. The results of this study provide further understanding of the in-vehicle air quality of air-conditioned coaches and can be used in the development of both specific and general rules regarding medium- and large-size coaches.

The Inflammation Response to DEHP through PPARγ in Endometrial Cells.

Epidemiological studies have shown the possible link between phthalates and endometrium-related gynecological diseases, however the molecular mechanism(s) behind this is/are still unclear. In the study, both primary cultured endometrial cells and an endometrial adenocarcinoma cell line (Ishikawa) were recruited to investigate the effects of di-(2-ethylhexyl) phthalate (DEHP) at human-relevant concentrations. The results showed that DEHP did not affect the viability of either type of cell, which showed different responses to inflammation. Primary cultured cells showed stronger inflammatory reactions than the Ishikawa cell line. The expression of inflammatory factors was induced both at the mRNA and protein levels, however the inflammation did not induce the progress of epithelial-mesenchymal transition (EMT) as the protein levels of EMT markers were not affected after exposure to either cell type. Further study showed that the mRNA levels of peroxisome proliferator-activated receptor gamma (PPARγ) wereup-regulated after exposure. In all, our study showed that human-relevant concentrations of DEHP could elicit the inflammatory response in primary cultured endometrial cells rather than in Ishikawa cell line. PPARγ may act as the mediating receptor in the inflammation reaction.