Encapsulation of Ultrafine Metal-Organic Framework Nanoparticles within Multichamber Carbon Spheres by a Two-Step Double-Solvent Strategy for High-Performance Catalysts.

Carbon-encapsulated metal-organic framework (MOF) composite is one kind of emerging new catalyst with high efficiency and has gained much attention. However, for this kind of composite catalyst, the key to improving its catalytic activity and durability is to realize the effective dispersion of MOF nanoparticles (NPs) and enhance the interaction between MOF NPs and the carbon matrix, which remain a significant challenge. Herein, ultrafine MOF NPs within multichamber carbon spheres (MOF@MCCS), for the first time, have been rationally synthesized by a two-step double-solvent strategy for high-performance catalysts. The precise loading of guest MOFs can be achieved by adjusting the multichamber structure and calcination extent of the multichamber polymer (MCP), and the particle size of MOFs can be as low as 13.2 nm. Due to the formation of abundant carbon defects in the pyrolysis process of MCPs, the special structure and synergistic effect make the material exhibit higher catalytic activity and durability. More importantly, this method is universal and can be extended to different MOF systems. The two-step double-solvent strategy not only prepares a unique structure of MOF@MCCS-type host-guest-encapsulated catalysts but also provides a new idea for the design of high-efficiency catalysts with better performance and higher durability.

PARP-1 promotes autophagy via the AMPK/mTOR pathway in CNE-2 human nasopharyngeal carcinoma cells following ionizing radiation, while inhibition of autophagy contributes to the radiation sensitization of CNE-2 cells.

It was previously reported that poly-(adenosine diphosphate-ribose) polymerase-1 (PARP-1) regulated ionizing radiation (IR)-induced autophagy in CNE-2 human nasopharyngeal carcinoma cells. The present study aimed to investigate whether PARP-1-mediated IR-induced autophagy occurred via activation of the liver kinase B1 (LKB1)/adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway in CNE-2 cells. In addition, the effect of PARP-1 and AMPK inhibition on the radiation sensitization of CNE-2 cells was investigated. CNE-2 cells were treated with 10 Gy IR in the presence or absence of the AMPK activator 5-amino-1-ß-D-ribofuranosyl-1H-imid-azole-4-carboxamide (AICAR). In addition, IR-treated CNE-2 cells were transfected with lentivirus-delivered small-hairpin RNA or treated with the AMPK inhibitor Compound C. Western blot analysis was used to assess the protein expression of PARP-1, phosphorylated (p)-AMPK, microtubule-associated protein 1 light chain 3 (LC3)-II and p-P70S6K. Cell viability and clone formation assays were performed to determine the effect of PARP-1 silencing and AMPK inhibition on the radiation sensitization of CNE-2 cells. The results showed that IR promoted PARP-1, p-AMPK and LC3-II protein expression as well as decreased p-P70S6K expression compared with that of the untreated cells. In addition, AICAR increased the expression of p-AMPK and LC3-II as well as decreased p-P70S6K expression compared with that of the IR-only group; however, AICAR did not increase PARP-1 expression. Furthermore, PARP-1 gene silencing decreased the expression of PARP-1, p-AMPK and LC3-II as well as increased p-P70S6K expression. Compound C decreased p-AMPK and LC3-Ⅱ expression as well as increased p-P70S6K expression; however, Compound C did not increase PARP-1 expression. Western blot analysis detected limited expression of p-LKB1 in all treatment groups. Cell viability and clone formation assays revealed that PARP-1 or AMPK inhibition reduced the proliferation of CNE-2 cells following IR. In conclusion, the present study demonstrated that PARP-1 promoted autophagy via the AMPK/mTOR pathway; in addition, PARP-1 or AMPK inhibition contributed to the radiation sensitization of CNE-2 cells following IR. However, it remains to be elucidated whether PARP-1 is an upstream mediator of the LKB1 pathway in CNE­2 cells following IR.

RNAi-mediated knockdown of the c-jun gene sensitizes radioresistant human nasopharyngeal carcinoma cell line CNE-2R to radiation.

This study aimed to investigate the effect of RNA interference (RNAi)-mediated downregulation of the expression of the c-jun gene (a proto-oncogene) on the radiosensitivity of a radioresistant human nasopharyngeal carcinoma cell line (CNE-2R) and to validate its potential as an anticancer target. A lentiviral vector with c-jun small hairpin RNA (shRNA) was constructed and transfected into CNE-2R cells. The gene silencing efficiency of these recombinants was confirmed by RT-PCR and western blotting. Radiosensitivity, cell proliferation, cell cycle profile and apoptosis were assessed using colony formation assay, CCK-8 assay and flow cytometry, respectively. The lentiviral shRNA efficiently knocked down the expression of c-jun at both the mRNA and protein levels (P<0.05). c-jun-downregulated CNE-2R cells exhibited significantly decreased cell proliferation and enhanced radiosensitivity compared to the control group (P<0.05), and the effects were likely due to G2/M phase arrest and enhanced cell apoptosis. These data provide evidence that c-jun may be involved in the radioresistance of nasopharyngeal carcinoma (NPC) and knockdown of the c-jun gene may be a potential strategy to enhance the radiation sensitivity of NPC.