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P-doped TiO 2 nanoparticles were synthesized by the sol-gel method with various H 3 PO 4 amounts. The samples were calcinated at different temperature and charactered by XPS, ICP, XRD, SEM, Raman, FTIR, and UV-vis methods, so that the formation process of phosphate species could be inspected. The XRD results show that P species hinder the particle growth of anatase and increase the anatase-to-rutile phase transformation temperature to more than 900 °C, and a new titanyl phosphate, Ti 5 O 4 (PO 4 ) 4 , was observed in P-doped TiO 2 when calcined at 1000 °C. The UV-vis results indicate that the P species is likely to have two different states, leading to the variety of visible-light photocatalytic activity and band gap energy of P-doped TiO 2 . One state is the "separated phase". In this state, the P/Ti ratio is very low so that the P species is surrounded by TiO 2 . The "separated phase" of P species introduces oxygen into TiO 2 lattice and hence causes a red-shift of the adsorption band edge of anatase, leading to the increased visible-light photocatalytic activity of P-doped TiO 2 . The other state is the "congregated phase". It appears at the micro region where the ratio of P/Ti is high enough to make the TiO 2 clusters isolated by P species. The "congregated phase" of P species acts as the interface phase between TiO 2 clusters and strongly retards the crystal growth of anatase, resulting in the widened band gap of P-doped TiO 2 . Furthermore, a possible mechanism was also proposed to explain the formation of the two phases during the sol-gel process. The results indicate that in order to improve the visible-light photocatalytic activity of P-doped TiO 2 the percentage of "separated phase" in P species needs to be enhanced.

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Background Non-small cell lung cancer (NSCLC) is a common malignant tumor in humans. Long non-coding RNA (lncRNA) involved in cancer progression has been reported frequently. The objective of this study was to investigate the role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and explore a novel mechanism in NSCLC development. Materials and Methods The expression of MALAT1, copper metabolism MURR1 domain-containing 8 ( COMMD8 ) and microRNA-613 (miR-613) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of COMMD8, Cyclin D1, Ki67, B cell lymphoma/leukemia-2 (Bcl-2), Bcl-2 associated X protein (Bax), lactate dehydrogenase A (LDHA), CD63 and CD81 were determined by Western blot. Cell proliferation, the number of colonies and cell apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation and flow cytometry assays, respectively. Glycolysis was distinguished based on glucose consumption, lactate production and LDHA activity. The role of MALAT1 in vivo was verified by animal experiments. The relationship between miR-613 and MALAT1 or COMMD8 was predicted by the bioinformatics tool starbase and verified by dual-luciferase reporter assay. The exosomes were isolated using the corresponding kit and identified by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). Results MALAT1 and COMMD8 were aberrantly upregulated in NSCLC tissues and cells. MALAT1 or COMMD8 knockdown blocked cell proliferation, colony formation and glycolysis but accelerated cell apoptosis in vitro. Besides, MALAT1 knockdown reduced tumor growth in vivo. We found that miR-613 was a target of MALAT1, and miR-613 could bind to the 3ʹ untranslated region (3ʹUTR) of COMMD8 . MALAT1 regulated the expression of COMMD8 by absorbing miR-613. Moreover, the extracellular MALAT1 was transmitted by wrapping into exosomes. Conclusion MALAT1 promoted malignant activities of NSCLC cells through targeting miR-613/ COMMD8 axis, and exosome-mediated transfer of NSCLC might be a novel approach for NSCLC treatment.

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