Screening of structural and functional alterations in duckweed (Lemna minor) induced by per- and polyfluoroalkyl substances (PFASs) with FTIR spectroscopy.

As a class of common emerging pollutants, per- and polyfluoroalkyl substances (PFASs) and their alternatives have been widely detected in various environmental matrices, exhibiting a great threat to the ecological environment and human health. Nevertheless, changes in biomolecular structure and function of duckweed caused by PFASs and their alternatives remain unknown thus far. Herein, the effects of four PFASs, including two common legacy PFASs (perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA)) and two PFASs alternatives (perfluorobutane sulfonic acid (PFBS) and 1H,1H,2H, 2H-perfluorooctane sulfonic acid (6:2 FTS)) on duckweed (Lemna minor) at biochemical level were investigated with Fourier transform infrared spectroscopy (FTIR). Although no obvious inhibitions were observed in the growth of L. minor with PFASs exposure at three levels of 1 µg L-1, 100 µg L-1, and 10 mg L-1, significant structural and functional alterations were induced at the biochemical level. In response to PFASs exposure, lipid peroxidation, proteins aggregation and α-helix to ß-sheet transformation of the protein conformation, as well as changes of DNA conformations were detected. Moreover, alterations in lipid, protein, and DNA were proved to be concentration-related and compound-specific. Compared to the two legacy PFASs (PFOS and PFOA), alternative ones exhibited greater effects on the biological macromolecules of L. minor. The findings of this study firstly reveal structural and functional alterations in L. minor induced by PFASs exposure, providing further understanding of their toxicity effects.

MIR22HG Regulates the Proliferation, Epithelial-Mesenchymal Transition, and Apoptosis in Colorectal Carcinoma.

Background: Recent investigations have suggested that long noncoding RNA (lncRNA) MIR22HG is commonly dysregulated in multiple types of malignancies. Nevertheless, the role of these MIR22HG in human colorectal carcinoma (CRC) are not well explored. Materials and Methods: Quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH) assay were used to measure the expression of MIR22HG. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and migration, as well as invasion assays, were utilized to determine the roles of MIR22HG on growth, apoptosis, migration, and invasiveness of CRC cell. The expression of E-cadherin and N-cadherin was measured using Western blotting and immunohistochemistry staining assay. CRC cell growth in vivo was analyzed using nude mice xenograft. Results: The qPCR and ISH assay revealed that MIR22HG was downregulated in CRC sample compared with in normal tissue. MIR22HG was also significantly downexpressed in CRC cells compared with that in normal colonic epithelial cell line. Overexpression of MIR22HG inhibited the growth, migration ability, and invasiveness of CRC cell in vitro. In addition, MIR22HG suppressed the epithelial-mesenchymal transition (EMT) and induced the apoptosis of human CRC cell. Moreover, the authors demonstrated that MIR22HG inhibited the tumor growth of CRC cell and regulated the expression of EMT markers (E-cadherin and N-cadherin) in vivo. Conclusion: Altogether, these results imply that lncRNA MIR22HG restrained the aggressive phenotypes of CRC cell.