Molecular and Cellular Probes最新文献

Recently, the microbiome has been gaining significant attention in the healthcare sector as a next-generation factor. However, there remains a substantial gap in our understanding of the fundamental mechanisms of microbes, particularly regarding the effector microbial products exchanged between the microbiota and the host. Consequently, research on microbial extracellular vesicles (MEVs) has increased. MEVs, which are nano-sized, can circulate throughout the body and penetrate the bloodstream, carrying diverse information. Consequently, they are increasingly being utilized in medical applications. Additionally, AI technologies are being utilized in medicine. The combination of MEVs and AI technology is being explored for the development of algorithm-based in vitro diagnostics (IVD). Therefore, this study aims to review the integration of MEVs and AI technology as diagnostic tools for personalized medicine. This paper reviewed the MEV-based algorithms developed by a variety of human samples and AI technology. Additionally, most of MEV-based diagnostic models showed higher clinical performance. Several important factors are crucial for accurate diagnosis. First, optimizing sample types according to specific diseases is essential. Second, AI technology with higher diagnostic power yields more accurate results. Finally, incorporating additional markers can enhance diagnostic power. However, applying this tool in situ faces several limitations, including method standardization, sample size, and analysis techniques. In the future, we anticipate that research on MEVs will advance our understanding of their role in disease and establish the foundation for precision medicine strategies.

In gastric cancer (GC), tumor cell metastasis to lymph node may occur, and can be impacted by synaptojanin 2 (SYNJ2). Herein, we explored the mechanism of SYNJ2 in the progress of GC. SYNJ2 level in GC tissues was predicted by GEPIA database. After GC cells were transfected with short hairpin RNA against SYNJ2 (shSYNJ2), shGRB2, SYNJ2 overexpression plasmid and GRB2 overexpression plasmid, the mRNA levels of SYNJ2 and growth factor receptor-bound protein 2 (GRB2) in GC cells were quantified by qRT-PCR. CCK-8, flow cytometry, wound healing, transwell and tube formation assays were performed for detecting viability, apoptosis, migration, invasion and angiogenesis of GC cells. Protein levels of GRB2, vascular endothelial growth factor (VEGF), E-Cadherin, N-Cadherin and Vimentin in GC cells were measured by Western blot. The relationship between SYNJ2 and GRB2 was assessed by Co-immunoprecipitation (CO-IP) assay. SYNJ2 was highly expressed in GC tissues and cells. SYNJ2 overexpression promoted viability, migration, invasion, angiogenesis and GRB2 level, and inhibited apoptosis of GC cells, while shSYNJ2 exhibited opposite effects. GRB2 overexpression boosted yet shGRB2 suppressed cell migration, invasion and angiogenesis. Notably, SYNJ2 could interact with GRB2. GRB2 overexpression and shGRB2 reversed the effects of shSYNJ2 and overexpressed SYNJ2 on cell migration, invasion and angiogenesis and levels of metastasis-related proteins, respectively. In conclusion, SYNJ2 promotes GC cell metastasis and angiogenesis by up-regulating GRB2.

Active neutrophils play a variety of roles in both innate and adaptive immune responses, and one of the most vital roles is the formation and release of neutrophil extracellular traps (NETs). NETs are created when neutrophils release their chromatin contents to get and eradicate pathogenic organisms essentially. While NET helps fight bacteria, viruses, parasites, and infections, it is also linked to asthma, atherosclerosis, and cancer metastasis. Thus, understanding the molecular mechanisms behind NETosis formation and its inhibition is crucial for developing safe and effective therapies. This systematic review aims to identify the list of miRNAs that are associated with the formation of NETosis and illustrate the mechanism of action by classifying them based on their expression site. Moreover, it summarizes the list of miRNAs that can be targeted therapeutically to reduce NETosis in various disorders. The current study entailed the searching of PubMed and Google Scholar for articles related to the research topic role of miRNAs in NETosis in all types of disorders. The search terms and phrases included "NETs," "neutrophil extracellular traps," "NETosis," "miRNA," "miR," and "micro-RNA." The search was limited to articles published in English since October 2024 in both databases. Following a review of 23 papers, 19 of them met the inclusion and exclusion criteria of this study. Four papers have been removed as they are duplicated or do not meet our criteria. According to the published articles till October 2024, there are 14 miRNAs involved in the molecular pathway of NETosis which are miR-155, miR-1696, miR-7, miR-223, miR-146a, miR-142a-3p, miR-3146, miR-505, miR-4512, miR-15b-5p, miR-16-5p, miR-26b-5p, miR-125a-3p and miR-378a-3p. Moreover, eight miRNAs have been identified as possible therapeutic targets for the suppression of NETosis based on in-vivo studies carried out in various organisms, which are miR-155, miR-146a, miR-1696, miR-223, miR-142a-3p, miR-3146, miR-4512, miR-16-5p. Different miRNAs that are expressed inside or outside of neutrophils can regulate and influence NETosis. Eight miRNAs have also been identified as potential therapeutic targets, which can be utilized to inhibit the molecular pathways associated with NETosis and prevent its negative effects, such as asthma, atherosclerosis, cancer metastasis, and cancer recurrence. However, further human-based research is necessary to completely understand the role of miRNAs in the development of NETosis in humans.