Fen Zhang,Wei Chen,Lingling Wang,Weiguo Song,Yin Hu
Preparation of nano-rod aluminosilicate Mazzit (MAZ) zeolite under low-cost and environmental-friendly route is attractive, but still challenging. Herein, we report a green route for synthesizing nano-rod MAZ zeolite (MAZ-N) using low-cost and environmental-friendly choline chloride as template. Various characterizations including powder X-ray diffraction (XRD), scanning electron microscope (SEM), N2sorption, and thermogravimetry-differential thermal analysis (TG-DTA) show that MAZ-N samples have good crystallinity and uniform porous structures. Furthermore, the crystallization process and impact of synthesis conditions of MAZ-N samples have been investigated in detail. These results suggest the potential applications of MAZ-N zeolites as supporting catalyst compounds in industrial processes.Keywords:zeolites;low-cost;environmental-friendly;aluminosilicate MAZ;nano-rod
Tao Wang,Xu Zhu,Kai Wang,Jianglun Li,Xiao Hu,Peng Lin,Jian Zhang
Background Cisplatin remains a common chemotherapy drug for lung adenocarcinoma (LUAD) in clinical treatment. Long-term use of cisplatin in patients may lead to acquired drug resistance, resulting in poor prognoses of patients. NEIL3 was a glycosylase-encoding gene highly expressed in LUAD. NEIL3 can repair telomerase DNA damage in the S phase. Nevertheless, there are few reports on whether NEIL3 is involved in cisplatin resistance and its related mechanisms in LUAD. Methods The expression of NEIL3 in LUAD patients was analyzed by bioinformatics. The regulator upstream of NEIL3 was predicted via hTFtarget. The possibly involved pathways of NEIL3 were obtained by performing Gene Set Enrichment Analysis. qRT-PCR and western blot were applied to test the expression level of genes and protein LUAD cells. Dual - luciferase assay and chromatin immunoprecipitation (ChIP) assay were conducted to validate the binding relationship between MAZ and NEIL3. Cell function assays were performed to test the DNA damage, cell viability, cell migration and invasion, and cell cycle of LUAD cells in the treatment group. Results NEIL3 and its upstream regulatory factor MAZ were highly expressed in LUAD tissue, and NEIL3 was enriched in cell cycle and mismatch repair pathways. Dual-luciferase assay and ChIP assay proved that MAZ could target NEIL3. Cell experiments identified that MAZ/NEIL3 axis could repress DNA damage to advance cisplatin resistance of cancer cells, and foster cell migration and invasion in LUAD. Conclusion MAZ-activated NEIL3 could propel the cisplatin resistance in LUAD by repressing DNA damage.
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