Int J Med Sci
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Recurrent miscarriage (RM) is a pregnancy complication associated with dysregulation of the maternal-fetal interface. We aimed to identify dysfunctional interactions between trophoblast cells and decidual immune cells in RM. We downloaded single-cell RNA sequencing (scRNA-seq) datasets (GSE214607) from the Gene Expression Omnibus (GEO) datasets for further analysis using the R software. ⋯ We divided trophoblast cells into three types and analyzed their interactions with decidual immune cells. Additionally, we re-clustered NK&T cells and macrophages, identified differentially expressed genes (DEGs), enriched their functions, and compared the cell interactions with trophoblast cells in each cell type. Our single-cell atlas of the maternal-fetal interface revealed alterations in the cellular organization of the decidua and placenta, cell type-specific transcriptome, and cell communication between immune and non-immune cells in RM, which are critical for illuminating the pathophysiology of RM.
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[This corrects the article DOI: 10.7150/ijms.25656.].
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Objective: Gastric cancer (GC) has high morbidity and mortality due to inefficient early screening. Therefore, we are searching for more sensitive and specific diagnostic markers for GC. tRNA-derived small RNAs are novel non-coding small RNAs with good abundance and stable presence in body fluids, which may play multiple biological regulatory roles. In this study, we aimed to find a potential biomarker with high accuracy in tRNA-derived small RNAs that can help diagnose GC. ⋯ Results: tRF-27-FDXXE6XRK45 expression levels, significantly upregulated in tissues and sera of GC patients and decreased after radical GC surgery, were correlated with the degree of differentiation, depth of tumor infiltration, TNM stage, lymph node metastasis, and nerve/vascular invasion. In comparison with current GC diagnostic markers, tRF-27-FDXXE6XRK45 displayed better efficacy. Conclusions: tRF-27-FDXXE6XRK45, with high diagnostic efficacy, can distinguish GC patients from gastritis patients and healthy donors, suggesting that tRF-27-FDXXE6XRK45 may be a promising candidate as a diagnostic marker for GC.
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Periodontal ligament stem cells (PDLSCs) are important candidate seed cells for alveolar bone tissue engineering. Dasatinib is a tyrosine kinase inhibitor, and its influence on the osteogenic differentiation of mesenchymal stem cells is a controversial topic. The present study explored the effects of different concentrations of dasatinib on the proliferation and osteogenic differentiation of PDLSCs and tentatively revealed the related mechanism. ⋯ ALP staining, alizarin red staining, and western blot proved that low concentrations of dasatinib (1 nM) promoted the osteogenic differentiation of PDLSCs, while high concentrations of dasatinib inhibited it. The negative effects of dasatinib on osteogenic differentiation were reversed when EID3 was knocked down, suggesting that EID3 mediates the regulation of dasatinib on the osteo-differentiation of PDLSCs. Taken together, high concentrations of dasatinib inhibited the proliferation and osteogenic differentiation of PDLSCs through Erk and EID3 signals, while low concentrations of dasatinib could be a potential method to enhance the bone regeneration ability of PDLSCs.
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Long non-coding RNAs are considered to be key regulatory factors of oncogenesis and tumor progression. It is reported that LINC00460 plays the role of oncogene in some tumors. However, LINC00460's role and mechanism of action in pancreatic cancer have not yet been fully elucidated. ⋯ Furthermore, LINC00460 functioned as an miR-4689 sponge to regulate the downstream target gene UBE2V1, enhancing the stability of mutant p53 in pancreatic cancer cells. LINC00460 also further promotes pancreatic cancer development by sequestering USP10, a cytoplasmic ubiquitin-specific protease that deubiquitinates p53 and enhances its stability. Collectively, our study demonstrated that LINC00460 is a hypoxia-induced lncRNA that plays the role of oncogene in pancreatic cancer by modulating the miR-4689/UBE2V1 axis, sequestering USP10, and ultimately enhancing the stability of mutant p53.