Objective Osteosarcoma (OS) is characterized by high levels of the tumour‐associated inflammatory microenvironment. Moreover, in approximately 60% of OS, telomere length is maintained by alternative lengthening of telomeres (ALT) pathway. Whether the ALT pathway can be exploited for OS therapeutic treatment and how the OS inflammatory microenvironment influences the anti‐cancer drug effect remains unknown. Here, we examined the biological effects of TMPyP4 and cisplatin in the inflammatory microenvironment of OS cells. Materials and methods Immunofluorescence in situ hybridization (IF‐FISH) and C‐circle experiments were used to detect the G‐quadruplex and ALT activity. The redox potential of single guanine, G‐quadruplex and G‐quadruplex/TMPyP4 was evaluated by the lowest unoccupied molecular orbital energy (LUMO), zeta potential and cyclic voltammetry. Cell viability, flow cytometry and apoptosis, Western blot, comet assay, adhesion, transwell and scratch experiments were performed to compare the anti‐tumour proliferation and migration effects of TMPyP4 and cisplatin in the inflammatory microenvironment. Results This study indicated that compared with cisplatin, TMPyP4 could induce the formation of human telomeres and FAK G‐quadruplex in vitro and in vivo, and TMPyP4‐treated OS cells showed fewer extrachromosomal C‐circles and fewer ALT‐associated promyelocytic leukaemia bodies. Consequently, the ALT activity and FAK‐related cell migration were suppressed by TMPyP4. Mechanistically, the formation of G‐quadruplex resulted in both lower redox potential than G within the genome and FAK transcription inhibition, and TMPyP4 could enhance this phenomenon, especially in the inflammatory microenvironment. Conclusions Our results reveal that TMPyP4 is more suitable for OS treatment than cisplatin.

Cancer is one of the diseases that threatens human health and is a leading cause of mortality worldwide.High levels of reactive oxygen species (ROS) have been observed in cancer tissues compared with normal tissues in vivo, and it is not yet known how this in uences chemotherapeutic drug action. Cationic porphyrin 5,10,15,20-tetra-(N-methyl-4-pyridyl) porphyrin (TMPyP4) is a photosensitizer used in photodynamic therapy (PDT) and a telomerase inhibitor used in the treatment of telomerase-positive cancer. Here, we investigated the anticancer activity of TMPyP4 in A549 and PANC cells cultured in H 2 O 2 .The results showed that compared to TMPyP4 alone, the combination of TMPyP4 and H 2 O 2 exhibited sensitization effects on cell viability and colony formation inhibition and apoptosis in A549 and PANC cells but had no effect in human normal MIHA cells. Mechanistically, the combination of TMPyP4 and H 2 O 2 activates high ROS and mitochondrial membrane potential in A549 and PANC cells, resulting in intense DNA damage and DNA damage responses. Consequently, compared to TMPyP4 alone, TMPyP4 and H 2 O 2 combined treatment upregulates the expression of BAX, cleaved caspase 3, and p-JNK, and downregulates the expression of Bcl-2 in A549 and PANC cells. Taken together, these data suggested that H 2 O 2 enhanced the anticancer activity of TMPyP4-mediated ROS-dependent DNA damage and related apoptotic protein regulation, revealing that the high ROS tumor microenvironment plays an important role in chemotherapeutic drug action.

As the capacity of lithium-ion batteries (LIBs) with commercial graphite anodes is gradually approaching the theoretical capacity of carbon, the development of silicon-based anodes, with higher energy density, has attracted great attention. However, the large volume variation during its lithiation/de-lithiation tends to lead to capacity decay and poor cycling performance. While rationally designed silicon/carbon (Si/C) anodes can exhibit higher specific capacity by virtue of silicon and high electrical conductivity and volume expansion suppression by virtue of carbon, they still show poor cycling performance with low initial coulombic efficiency. This review focuses on three strategies for structural design and optimization of Si/C anodes, i.e., carbon-coated structure, embedded structure and hollow structure, based on the recent researches into Si/Canodes and provides deeper insights into the problems that remain to be addressed.

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The exploitation of high‐performance, durable, and low‐cost oxygen reduction reaction (ORR) electrocatalysts is crucial for energy storage and convert devices. Herein, a core‐shell structured catalyst (FeNx@graphite carbon) is developed by coaxial electrospinning. The resulting nanofibers combines the distinguished activity of FeNx and the good conductivity and stability of graphite carbon. This unique core‐shell structure with potential synergistic interaction leads to high activity and outstanding stability. As an excellent cathode catalyst for the Zn‐air battery, FeNx@graphite carbon displays an outstanding open‐circuit voltage (1.592 V), a high peak power density (100 mW cm−2) and stable rechargeability (30 h), outperforming that of Pt/C assembled Zn‐air battery. Our work provides a guide to rational design for achieving both high ORR activity and good stability.

Cancer is one of the diseases that threatens human health and is a leading cause of mortality worldwide. High levels of reactive oxygen species (ROS) have been observed in cancer tissues compared with normal tissues in vivo, and it is not yet known how this influences chemotherapeutic drug action. Cationic porphyrin 5,10,15,20-tetra-(N-methyl-4-pyridyl) porphyrin (TMPyP4) is a photosensitizer used in photodynamic therapy (PDT) and a telomerase inhibitor used in the treatment of telomerase-positive cancer. Here, we investigated the anticancer activity of TMPyP4 in A549 and PANC cells cultured in H2O2. The results showed that compared to TMPyP4 alone, the combination of TMPyP4 and H2O2 exhibited sensitization effects on cell viability and colony formation inhibition and apoptosis in A549 and PANC cells but had no effect in human normal MIHA cells. Mechanistically, the combination of TMPyP4 and H2O2 activates high ROS and mitochondrial membrane potential in A549 and PANC cells, resulting in intense DNA damage and DNA damage responses. Consequently, compared to TMPyP4 alone, TMPyP4 and H2O2 combined treatment upregulates the expression of BAX, cleaved caspase 3, and p-JNK, and downregulates the expression of Bcl-2 in A549 and PANC cells. Taken together, these data suggested that H2O2 enhanced the anticancer activity of TMPyP4-mediated ROS-dependent DNA damage and related apoptotic protein regulation, revealing that the high ROS tumor microenvironment plays an important role in chemotherapeutic drug action.