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NFBD1, a signal amplifier of the p53 pathway, is vital for protecting cells from p53-mediated apoptosis and the early phase of DNA damage response under normal culture conditions. Here we investigated its expression in patients with nasopharyngeal carcinoma (NPC), and we describe the biological functions of the NFBD1 gene. We found that NFBD1 mRNA and protein were more highly expressed in NPC tissues than in nontumorous tissues. To investigate the function of NFBD1, we created NFBD1-depleted NPC cell lines that exhibited decreased cellular proliferation and colony formation, an increase in their rate of apoptosis, and an enhanced sensitivity to chemotherapeutic agents compared with in vitro controls. However, N-acetyl cysteine (NAC) and downregulation of p53 expression could partially reverse the apoptosis caused by the loss of NFBD1. Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway. Using a xenograft model in nude mice, we showed that silencing NFBD1 also significantly inhibited tumor growth and led to apoptosis. Taken together, our data suggest that inhibition of NFBD1 in NPC could be therapeutically useful.

NFBD1, a signal amplifier of the p53 pathway, is vital for protecting cells from p53-mediated apoptosis and the early phase of DNA damage response under normal culture conditions. Here we investigated its expression in patients with nasopharyngeal carcinoma (NPC), and we describe the biological functions of the NFBD1 gene. We found that NFBD1 mRNA and protein were more highly expressed in NPC tissues than in nontumorous tissues. To investigate the function of NFBD1, we created NFBD1-depleted NPC cell lines that exhibited decreased cellular proliferation and colony formation, an increase in their rate of apoptosis, and an enhanced sensitivity to chemotherapeutic agents compared with in vitro controls. However, N -acetyl cysteine (NAC) and downregulation of p53 expression could partially reverse the apoptosis caused by the loss of NFBD1. Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway. Using a xenograft model in nude mice, we showed that silencing NFBD1 also significantly inhibited tumor growth and led to apoptosis. Taken together, our data suggest that inhibition of NFBD1 in NPC could be therapeutically useful. [ABSTRACT FROM AUTHOR]

• F-PCP NPs for rheumatoid arthritis are developed. • F-PCP NPs has obtained excellent photothermal therapy performance. • F-PCP NPs actively target M1 macrophages to reduce its proliferation. Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint hypoxia and the proliferation of M1 macrophages. Therefore, relieving hypoxia and removing M1 macrophages will be a new direction in the treatment of RA. Folic acid (FA)-loaded PCP nanoparticles Fe-Co prussian blue analogue@CeO 2 @PDA (F-PCP) were used for in situ oxygen (O 2) production/chemodynamic/photothermal/treatment of RA. On one hand, PDA-mediated photothermal therapy also has a certain effect on the removal of proliferative M1 macrophages. On the other hand, under the irradiation of NIR laser, F-PCP has obtained excellent photothermal therapy (PTT) performance, which accelerates the Fenton/Fenton-like reaction to produce reactive oxygen species and O 2 , so as to achieve the chemodynamic therapy (CDT) that inhibits the proliferation of M1 macrophages. It is worth noting that the RA was improved by the synergistic action of CDT and PTT, and the generation of oxygen can alleviate RA hypoxia, which is a means to improve CDT. Therefore, the F-PCP NPs show great potential in improving the therapeutic effect of RA. [ABSTRACT FROM AUTHOR]

Insufficient hydrogen peroxide content in tumor cells, unsuitable pH and low efficiency of commonly used metal catalysts severely affect the efficiency of chemodynamic therapy, resulting in unsatisfactory efficacy of chemodynamic therapy alone. For this purpose, we designed a composite nanoplatform capable of targeting tumors and selectively degrading in the tumor microenvironment (TME) to address these issues. In this work, we synthesized Au@Co 3 O 4 nanozyme inspired by crystal defect engineering. The addition of Au determines the formation of oxygen vacancies, accelerates electron transfer, and enhances redox activity, thus significantly enhancing the superoxide dismutase (SOD)-like and catalase (CAT)-like catalytic activities of the nanozyme. Subsequently, we camouflaged the nanozyme using a biomineralized CaCO 3 shell to avoid damage to normal tissues by the nanozyme while effectively encapsulating the photosensitizer IR820, and finally the tumor targeting ability of the nanoplatform was enhanced by the modification of hyaluronic acid. Under near-infrared (NIR) light irradiation, the Au@Co 3 O 4 @CaCO 3 /IR820@HA nanoplatform not only visualizes the treatment with multimodal imaging, but also plays a photothermal sensitizing role through various strategies, while enhancing the enzyme catalytic activity, cobalt ion-mediated chemodynamic therapy (CDT) and IR820-mediated photodynamic therapy (PDT), and achieving the synergistic enhancement of reactive oxygen species (ROS) generation. [ABSTRACT FROM AUTHOR]

• Core-satellite self-assembly enhanced the intensity of hot spots in the nanogaps. • The Raman signal of adenine in the nanogaps was significantly amplified. • Pt-tipped Au triangular nanoprism catalyzes oxygen generation to alter tumor hypoxia. • Core-satellite nanoplatform enhanced the synergistic therapy of tumors. The detection and imaging of human telomerase in living cells is of great significance for early diagnosis and treatment of cancers. Herein, we designed a new promising target-induced self-assembled core-satellite (C-S) structure for label-free Raman detection and fluorescence imaging of telomerase in cancer cells and enhanced photothermal and photodynamic treatment of tumors. Nanoprobe would be triggered by telomerase to form C-S structure to improve the intensity of hot spots and thus to generate intense SERS signal change of adenine (A) for label free Raman detection of telomerase, then the signal of chlorin e6 (Ce6) would be released for in situ fluorescence imaging. Our experimental findings proved that such a strategy exhibited great sensitivity and selectivity for telomerase. In addition, the Pt nanozymes decorated on the tip of Au TNPs showed good catalase-like capacity and stability which can convert endogenous H 2 O 2 to produce O 2 to avoid cell hypoxia and promote the generation of cytotoxic singlet oxygen (1O 2) for enhanced photodynamic therapy of tumors. This nanoprobe was successfully employed for in situ imaging of telomerase in different kinds of cells and for combination therapy of tumors. It further proves that this is a new biological strategy with far-reaching significance for early cancer diagnosis and treatment. [ABSTRACT FROM AUTHOR]