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"Li, Yanjing"
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Book
The caspase-3/GSDME signal pathway as a switch between apoptosis and pyroptosis in cancer
Apoptosis has long been recognized as a mechanism that kills the cancer cells by cytotoxic drugs. In recent years, studies have proved that pyroptosis can also shrink tumors and inhibit cells proliferation. Both apoptosis and pyroptosis are caspase-dependent programmed cell death pathways. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. When GSDME is highly expressed, the active caspase-3 cuts it and releases the N-terminal domain to punch holes in the cell membrane, resulting in cell swelling, rupture, and death. When the expression of GSDME is low, it will lead to the classical mechanism of tumor cell death, which is apoptosis. More interestingly, researchers have found that GSDME can also be located upstream of caspase-3, connecting extrinsic, and intrinsic apoptotic pathways. Then, promoting caspase-3 activation, and forming a self-amplifying feed-forward loop. GSDME-mediated pyroptosis is correlated with the side effects of chemotherapy and anti-tumor immunity. This article mainly reviews the caspase-3/GSDME signal pathway as a switch between apoptosis and pyroptosis in cancer, to provide new strategies and targets for cancer treatment.
Journal Article
Prospects and challenges of dynamic DNA nanostructures in biomedical applications
The physicochemical nature of DNA allows the assembly of highly predictable structures via several fabrication strategies, which have been applied to make breakthroughs in various fields. Moreover, DNA nanostructures are regarded as materials with excellent editability and biocompatibility for biomedical applications. The ongoing maintenance and release of new DNA structure design tools ease the work and make large and arbitrary DNA structures feasible for different applications. However, the nature of DNA nanostructures endows them with several stimulus-responsive mechanisms capable of responding to biomolecules, such as nucleic acids and proteins, as well as biophysical environmental parameters, such as temperature and pH. Via these mechanisms, stimulus-responsive dynamic DNA nanostructures have been applied in several biomedical settings, including basic research, active drug delivery, biosensor development, and tissue engineering. These applications have shown the versatility of dynamic DNA nanostructures, with unignorable merits that exceed those of their traditional counterparts, such as polymers and metal particles. However, there are stability, yield, exogenous DNA, and ethical considerations regarding their clinical translation. In this review, we first introduce the recent efforts and discoveries in DNA nanotechnology, highlighting the uses of dynamic DNA nanostructures in biomedical applications. Then, several dynamic DNA nanostructures are presented, and their typical biomedical applications, including their use as DNA aptamers, ion concentration/pH-sensitive DNA molecules, DNA nanostructures capable of strand displacement reactions, and protein-based dynamic DNA nanostructures, are discussed. Finally, the challenges regarding the biomedical applications of dynamic DNA nanostructures are discussed.
Journal Article
Pyroptosis, a new bridge to tumor immunity
Pyroptosis refers to the process of gasdermin (GSDM)‐mediated programmed cell death (PCD). Our understanding of pyroptosis has expanded beyond cells and is known to involve extracellular responses. Recently, there has been an increasing interest in pyroptosis due to its emerging role in activating the immune system. In the meantime, pyroptosis‐mediated therapies, which use the immune response to kill cancer cells, have also achieved notable success in a clinical setting. In this review, we discuss that the immune response induced by pyroptosis activation is a double‐edged sword that affects all stages of tumorigenesis. On the one hand, the activation of inflammasome‐mediated pyroptosis and the release of pyroptosis‐produced cytokines alter the immune microenvironment and promote the development of tumors by evading immune surveillance. On the other hand, pyroptosis‐produced cytokines can also collect immune cells and ignite the immune system to improve the efficiency of tumor immunotherapies. Pyroptosis is also related to some immune checkpoints, especially programmed death‐1 (PD‐1) or programmed death‐ ligand 1 (PD‐L1). In this review, we mainly focus on our current understanding of the interplay between the immune system and tumors that process through pyroptosis, and debate their use as potential therapeutic targets. The immune response induced by pyroptosis activation is a double‐edged sword that affects all stages of tumorigenesis. On the one hand, the activation of inflammasome‐mediated pyroptosis and the release of pyroptosis‐produced cytokines alter the immune microenvironment and promote the development of tumors by evading immune surveillance. On the other hand, pyroptosis‐produced cytokines can also collect immune cells and ignite the immune system to improve the efficiency of tumor immunotherapies.
Journal Article
GNINA 1.3: the next increment in molecular docking with deep learning
Computer-aided drug design has the potential to significantly reduce the astronomical costs of drug development, and molecular docking plays a prominent role in this process. Molecular docking is an
in silico
technique that predicts the bound 3D conformations of two molecules, a necessary step for other structure-based methods. Here, we describe version 1.3 of the open-source molecular docking software
Gnina
. This release updates the underlying deep learning framework to PyTorch, resulting in more computationally efficient docking and paving the way for seamless integration of other deep learning methods into the docking pipeline. We retrained our CNN scoring functions on the updated CrossDocked2020 v1.3 dataset and introduce knowledge-distilled CNN scoring functions to facilitate high-throughput virtual screening with
Gnina
. Furthermore, we add functionality for covalent docking, where an atom of the ligand is covalently bound to an atom of the receptor. This update expands the scope of docking with
Gnina
and further positions
Gnina
as a user-friendly, open-source molecular docking framework.
Gnina
is available at
https://github.com/gnina/gnina
.
Scientific contributions
: GNINA 1.3 is an open source a molecular docking tool with enhanced support for covalent docking and updated deep learning models for more effective docking and screening.
Journal Article
Structural basis for activity regulation of MLL family methyltransferases
The mixed lineage leukaemia (MLL) family of proteins (including MLL1–MLL4, SET1A and SET1B) specifically methylate histone 3 Lys4, and have pivotal roles in the transcriptional regulation of genes involved in haematopoiesis and development. The methyltransferase activity of MLL1, by itself severely compromised, is stimulated by the three conserved factors WDR5, RBBP5 and ASH2L, which are shared by all MLL family complexes. However, the molecular mechanism of how these factors regulate the activity of MLL proteins still remains poorly understood. Here we show that a minimized human RBBP5–ASH2L heterodimer is the structural unit that interacts with and activates all MLL family histone methyltransferases. Our structural, biochemical and computational analyses reveal a two-step activation mechanism of MLL family proteins. These findings provide unprecedented insights into the common theme and functional plasticity in complex assembly and activity regulation of MLL family methyltransferases, and also suggest a universal regulation mechanism for most histone methyltransferases.
Crystal structures of the SET domains of MLL3 and a mutant MLL1 either unbound or complexed with domains from RBBP5 and ASH2L are determined; a combination of structural, biochemical and computational analyses reveals a two-step activation mechanism of MLL family proteins, which may be relevant for other histone methyltransferases.
Activation mechanism for MLL enzymes
The SET domain-containing MLL family proteins methylate histone 3 on lysine 4 (H3K4) and have key roles in transcriptional regulation. MLL proteins are catalytically inactive on their own, and have full activity only when bound in a complex with three factors: WDR5, RBBP5, and ASH2L. Yong Chen and colleagues determine crystal structures of the SET domains of MLL3 and a mutant MLL1 in unbound forms or complexed with domains from RBBP5 and ASH2L and the histone H3 substrate. Their results suggest that WDR5 is not directly involved in enzymatic stimulation, and a combination of structural, biochemical and computational analyses reveals a two-step activation mechanism which may be relevant for all histone methyltransferases.
Journal Article
RETRACTED ARTICLE: Dihydroartemisinin enhances the anti-tumour effect of photodynamic therapy by targeting PKM2-mediated glycolysis in oesophageal cancer cell
We, the Editors and Publisher of Journal of Enzyme Inhibition and Medicinal Chemistry, have retracted the following article:Mengru Jin, Luyao Shi, Dingyaun Zhang and Yanjing Li (2023) Dihydroartemisinin enhances the anti-tumour effect of photodynamic therapy by targeting PKM2-mediated glycolysis in oesophageal cancer cell, Journal of Enzyme Inhibition and Medicinal Chemistry, DOI: https://doi.org/10.1080/14756366.2023.2296695Since publication, significant concerns have been raised regarding the Western blot images, ethical oversight of the study, and the authorship of the article.When approached for an explanation, the authors provided responses to our queries and the original data but were unable to address all of the concerns raised.As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The corresponding author listed in this publication has been informed.We have been informed in our decision-making by our Editorial Policies and COPE guidelines.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as ‘Retracted’.
Journal Article
Tetrahedral Framework Nucleic Acid-Based Delivery of Resveratrol Alleviates Insulin Resistance: From Innate to Adaptive Immunity
HighlightsTetrahedral framework nucleic acid (tFNA)-based delivery of resveratrol (RSV) ameliorates the performance of RSV.tFNAs-RSV improve insulin sensitivity in high-fat diet-fed mice by promoting Treg and Th2 and suppressing Th1 and Th17, and switching macrophage from M1 to M2 phenotype both in vitro and in vivo. Obesity-induced insulin resistance is the hallmark of metabolic syndrome, and chronic, low-grade tissue inflammation links obesity to insulin resistance through the activation of tissue-infiltrating immune cells. Current therapeutic approaches lack efficacy and immunomodulatory capacity. Thus, a new therapeutic approach is needed to prevent chronic inflammation and alleviate insulin resistance. Here, we synthesized a tetrahedral framework nucleic acid (tFNA) nanoparticle that carried resveratrol (RSV) to inhibit tissue inflammation and improve insulin sensitivity in obese mice. The prepared nanoparticles, namely tFNAs-RSV, possessed the characteristics of simple synthesis, stable properties, good water solubility, and superior biocompatibility. The tFNA-based delivery ameliorated the lability of RSV and enhanced its therapeutic efficacy. In high-fat diet (HFD)-fed mice, the administration of tFNAs-RSV ameliorated insulin resistance by alleviating inflammation status. tFNAs-RSV could reverse M1 phenotype macrophages in tissues to M2 phenotype macrophages. As for adaptive immunity, the prepared nanoparticles could repress the activation of Th1 and Th17 and promote Th2 and Treg, leading to the alleviation of insulin resistance. Furthermore, this study is the first to demonstrate that tFNAs, a nucleic acid material, possess immunomodulatory capacity. Collectively, our findings demonstrate that tFNAs-RSV alleviate insulin resistance and ameliorate inflammation in HFD mice, suggesting that nucleic acid materials or nucleic acid-based delivery systems may be a potential agent for the treatment of insulin resistance and obesity-related metabolic diseases.
Journal Article
New Pyridinium Compound from Marine Sediment-Derived Bacterium Bacillus licheniformis S-1
The structural diversity of marine natural products is considered a potential resource for the pharmaceutical industry. In our study of marine-derived compounds, one bacterium Bacillus licheniformis S-1 was discovered to have the ability to produce bioactive natural products. After a further chemistry investigation, one novel 4-aminopyridinium derivative, 4-(dimethylamino)-1-(2S-((4hydroxybenzoyl)oxy)propyl)pyridin-1-ium (1), along with 15 known cyclic dipeptides (2–16) were isolated from the bacterium B. licheniformis S-1 derived from a shallow sea sediment. The structures of compounds 1–16 were elucidated through comprehensive NMR spectroscopic and specific optical rotation (OR) data analyses. Compound 6 showed antibacterial activity against Pseudomonas fulva with an MIC value of 50 µg/mL. This is the first study to discover a pyridinium derivative and cyclic dipeptides from B. licheniformis.
Journal Article
Research progress on the role of microbiome-immune-neurotransmitter network in post-stroke sleep disorders
Post-stroke sleep disorders, as a significant complication affecting patient rehabilitation, are closely associated with dysregulation of the microbiome-immune-neurotransmitter network. Following stroke, activation of the hypothalamic-pituitary-adrenal axis and sympathetic nervous system triggers intestinal barrier disruption (reduced tight junction proteins and intestinal permeability) along with microbial imbalance (decreased
and increased Enterobacteriaceae). Reduced short-chain fatty acids and lipopolysaccharide (LPS) translocation exacerbate systemic inflammatory responses and neurotransmitter imbalances (inhibited serotonin synthesis and excitotoxic glutamate production). These changes further disrupt circadian regulation by the hypothalamic suprachiasmatic nucleus, leading to reduced REM sleep and disrupted slow-wave sleep architecture. Future research should prioritize interventional strategies targeting the gut microbiota, such as probiotics, prebiotics, and fecal microbiota transplantation, integrated with multi-omics technologies and neural circuit modulation approaches, to elucidate the spatiotemporal dynamics of the microbiome-immune-neurotransmitter network and provide a theoretical basis for clinical translation. Restoring brain-gut axis homeostasis is expected to improve post-stroke sleep disorders and neurological functional outcomes in patients.
Journal Article