The tungsten-containing mesoporous molecular sieve WO 3 -SBA-15 (SBA: Santa Barbara Amorphous type materials) was prepared under conventional hydrothermal conditions in strong acidic solution using H 2 WO 4 as tungsten source, tetraethyl orthosilicate as silicon source, and a mixture of P123 tri-block copolymer (EO 20 PO 70 EO 20 ) and cetyltrimethylammonium bromide as structure-directing agent. The catalyst was tested for oxidative desulfurization and characterized by X-ray diffraction and nitrogen adsorption-desorption. The catalyst had the highest desulfurization performance (i.e., 91.3%) after oxidation under the following reaction conditions: 20 mL gasoline with 540 ppm sulfur, 6 mol H 2 O 2 /sulfur, reaction temperature 333 K, reaction time 80 min, and three extraction cycles.

BackgroundLung cancer is the leading cause of cancer-related morbidity and mortality all over the world. Surgery resection, radiotherapy, chemotherapy, immunotherapy and combined treatments have been discovered and well established for treatments. However, low survival rate of five years after clinical treatments mainly due to recurrence of stress-resistant cancer cells calls for better understanding and new ideas. Our project aimed to understand the forming process of stress resistant lung cancer cells after radiotherapy.MethodsTwo classic non-small cell lung cancer (NSCLC) cell lines A549 and H1299 initially were radiated with a 137Cs gamma-ray source with doses ranging from 0 to 12 Gy to generate radiation-resistant cancer cells. 8 Gy of radiation was regard as a standard dosage since it provides effective killing as well as good amount of survivals. The expression levels of autophagy-related proteins including Beclin-1, LC3-II and p62 were studied and measured by both western blot and quantitative real-time polymerase chain reaction (real-time RT-PCR).ResultsIncreased Beclin-1, LC3-II and decreased p62 have been observed in radiation-resistant cells indicating elevated autophagy level. Decreased miR-191 in radiation-resistant cells performed by Taqman qRT-PCR also has been seen. Two binding sites between Beclin-1 and miR-191 suggest potential association between.ConclusionsIt is reasonable to speculate that inhibition of miR-191 expression in lung cancer cells would contribute to the establishment of radiation-resistant cells via mediating cellular autophagy. Therefore, miR-191 is a potential target for therapy in treating radiation-resistant lung cancer.

Recent studies have demonstrated that acquisition of epithelial-mesenchymal transition (EMT) is associated with drug resistance in lung cancer cells. However, the underlying mechanisms are not fully elucidated. Emerging evidence suggests that microRNAs play a crucial role in controlling EMT. The aim of this study was to explore the potential role of miR-125b in governing EMT in paclitaxel-resistant (PR) lung cancer cells. To achieve this goal, we explored the role of miR-125b in regulation of EMT in stable PR lung cancer cells, namely A549-PR and H460-PR. We found that miR-125b was significantly downregulated in A549-PR and H460-PR cells. Notably, ectopic expression of miR-125b led to the reversal of EMT phenotype. Moreover, we found that miR-125b governed PR-induced EMT partly due to down-regulation of its target Sema4C. More importantly, overexpression of miR-125b or depletion of Sema4C sensitized PR cells to paclitaxel. Furthermore, stable overexpression miR-125b in A549-PR cells inhibited tumor xenograft growth in immunodeficient mice. Our study implied that up-regulation of miR-125b could be a novel approach to reverse chemotherapy resistance in lung cancers.

No abstract available.