ObjectivemicroRNAs are regulatory molecules regarded as important in the pathogenesis of different types of tumors. microRNA-216a (miR-216a-5p) has been identified as a tumor suppressor in multiple malignancies. However, the role of miR-216a-5p in the pathogenesis of small cell lung cancer (SCLC) remains obscure. The objective of this study was to investigate the role of the miR-216a-5p/Bcl-2 axis in SCLC pathogenesis.Materials and methodsAll the experimental methods used were as follows: microarray analysis, cell culture, transient, and stable gene transfection; real-time fluorescence PCR; Western blot; flow cytometry for cell cycle analysis; in vitro proliferation assay; in vitro wound healing experiment; in vivo xenograft model in nude mice; and dual luciferase reporter assay. All statistical analyses were carried out using GraphPad Prism 7 software. Statistical significance was analyzed by Student’s t-test or one-way ANOVA. P <0.05 (typically compared with the negative control group) was considered as significant and is marked with an asterisk in the figures.ResultsIn this study, we observed that miR-216a-5p is downregulated in SCLC cell lines compared to that in the normal human bronchial epithelial cell line 16-HBE. In vitro and in vivo experiments demonstrate that upregulation of miR-216a-5p significantly decreased cell growth and migration and its downregulation increased SCLC cell proliferation and migration and influenced the cell cycle. Using bioinformatics analyses, we predicted that the important antiapoptotic gene Bcl-2 is targeted by miR-216a-5p, and we identified a functional miR-216a-5p binding site in the 3′-UTR of Bcl-2 using luciferase reporter assay. Furthermore, we determined that suppression of miR-216a-5p modulated the expression of Bcl-2, Bax, and Bad proteins (Bcl-2 family proteins), while Bcl-2 knockdown abrogated the effect of miR-216a-5p downregulation on cell proliferation, cell migration, and the cell cycle.ConclusionTaken together, these findings suggest that miR-216a-5p regulates SCLC biology via Bcl-2 family proteins. Therefore, our study highlights the role of the miR-216a-5p/Bcl-2 axis in SCLC pathogenesis.

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In this study, a surface chemical-modified rice husk biochar with abundant amino groups and disulfide bonds for the removal of cadmium was prepared using cystamine dihydrochloride as a modification ligand and glutaraldehyde as a crosslinker. The biochars were characterized by Fourier transform infrared spectrometry (FTIR), elemental analysis, scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), thermogravimetry analysis (TGA), and nitrogen sorption (BET) before and after modification. The adsorption properties of the modified biochars for Cd (II) were investigated in detail via adsorption isotherm models, adsorption kinetics models, and selective adsorption experiments. The surfaces of the cystamine-modified biochars with granular nanopolymers of sufficient functional groups of primary amine and disulfide linkage rendered the biochar surface more conducive to electrostatic attraction and surface complexation. The theoretical maximum adsorption capacity of the modified biochars (81.02 mg g−1) was almost 10-fold greater than that of the raw biochars (8.347 mg g−1) for Cd (II). Besides, the cystamine-modified biochars had a better affinity for Cd (II) compared to other heavy metals (Zn, As, Cd, Co, Ni, Cr), showing six-fold greater affinity for Cd (II) than Zn2+. The results of this study indicate that the modification of biochars derived from rice husks shows great potential in the removal of Cd (II) from contaminated water.

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