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Enzyme cascade reactions in biological systems can effectively improve the catalytic performances owing to their high local concentration, efficient mass transfer and reduced intermediate decomposition. However, the disadvantages of high cost, low stability, and easy inactivation limit their practical applications in harsh environments. Nanozymes as the substitutes for enzymes not only have enzyme-like activities but also possess high stability, tunable catalytic property, and high pH/temperature tolerance, which have been intensively investigated for the establishment of biomimetic catalysis systems. In this review, we first summarized the recent development of the construction and advantage of the nanozyme-involved cascade reaction system. Then, the biomedical applications of the nanozyme-enhanced biomimetic cascade catalytic systems, including biosensing, therapies and antioxidation, were highlighted in detail. Finally, current challenges and future perspectives for nanozyme-activated cascade reactions are discussed and outlooked.

Methyltransferase-like 3 (METTL3) is involved in RNA metabolism through N6-methyladenosine (m6A) modification. However, whether METTL3 participates in the progression of breast cancer is unclear. Aberrant expression of Mammalian hepatitis B X-interacting protein (HBXIP) drives the aggressiveness of breast cancer. Here, we are interested in the potential links between HBXIP and METTL3 in breast cancer. We showed that the expression of METTL3 was positively related to that of HBXIP in clinical breast cancer tissues. Moreover, HBXIP could up-regulate METTL3 in breast cancer cells. Mechanistically, HBXIP modulated METTL3 by inhibiting miRNA let-7g, which down-regulated the expression of METTL3 by targeting its 3'UTR. Strikingly, we found that METTL3 promoted the expression of HBXIP through m6A modification. Furthermore, overexpressed HBXIP could rescue the inhibited-proliferation and enhanced-apoptosis induced by silencing of METTL3 in breast cancer cells. Thus, we conclude that HBXIP up-regulates METTL3 by suppressing let-7g, in which METTL3 increased HBXIP expression forming a positive feedback loop of HBXIP/let-7g/METTL3/HBXIP, leading to accelerated cell proliferation in breast cancer. Our finding provides new insights into the mechanism of the mutual regulation between HBXIP and METTL3 in the progression of breast cancer.

The investigation revealed the effects of dissolved oxygen on the stability of aerobic granular sludge (AGS) in a membrane bioreactor. The results indicated that the variation of dissolved oxygen heavily influenced the characteristics of AGS, and a suitable DO range (1.5–2.0 mg/L) was an important guarantee to keep the stability of the structure of AGS, but under a low DO value (0–0.5 mg/L), the amount of Saprospiraceae increased which causes the reduction of protein content. Besides, the protein tag, a protein function secreted by Enterobacter hormaechei, was enriched, and they degraded the structural protein, which was an important reason causing the structure of AGS damaged. The results of proteomics analyses also showed that the number of proteins involved in extracellular structure and nuclear structure function is zero, which implied that the proteins in TB-EPS were mainly engaged in various functions but not in structural composition.

We have reported that the oncoprotein hepatitis B virus X-interacting protein (HBXIP) acts as a novel transcriptional coactivator to promote proliferation and migration of breast cancer cells. Previously, we showed that HBXIP was able to activate nuclear factor-κB (NF-κB) in breast cancer cells. As an oncogene, the platelet-derived growth factor beta polypeptide (PDGFB) plays crucial roles in carcinogenesis. In the present study, we found that both HBXIP and PDGFB were highly expressed in breast cancer cell lines. Interestingly, HBXIP was able to increase transcriptional activity of NF-κB through PDGFB, suggesting that HBXIP is associated with PDGFB in the cells. Moreover, HBXIP was able to upregulate PDGFB at the levels of mRNA, protein and promoter in the cells. Then, we identified that HBXIP stimulated the promoter of PDGFB through activating transcription factor Sp1. In function, HBXIP enhanced the proliferation of breast cancer cells through PDGFB in vitro. Thus, we conclude that HBXIP upregulates PDGFB via activating transcription factor Sp1 to promote proliferation of breast cancer cells.

NPY and alphaMSH are expressed in distinct neurons in the arcuate nucleus of the hypothalamus, where alphaMSH decreases and NPY increases food intake and body weight. Here we use patch-clamp electrophysiology from GFP-labeled POMC and NPY neurons to demonstrate that NPY strongly hyperpolarized POMC neurons through the Y1R-mediated activation of GIRK channels, while the alphaMSH analog, MTII, had no effect on activity of NPY neurons. While initially NPY had similar effects on POMC neurons derived from ob/ob mice, further studies revealed a significant increase in desensitization of the NPY-induced currents in POMC neurons from ob/ob mice. This increase in desensitization was specific to NPY, as GABA(B) and microOR agonists showed unaltered desensitization in POMC neurons from ob/ob mice. These data reveal an intricate and asymmetric interplay between NPY and POMC neurons in the hypothalamus and have important implications for the delineation of the neural circuits that regulate feeding behavior.