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Small nucleolar RNA H/ACA Box 51 (SNORA51) is involved in progression of multiple cancers. However, its role in hepatocellular carcinoma (HCC) is still unclear. The aim of the present study was to analyze the expression of SNORA51 in HCC and its clinical significance. A total of 136 patients with HCC who underwent surgery from January 1, 2016 to December 31, 2018 were included. The expression of SNORA51 in cancer tissues and adjacent tissues was compared using reverse transcription-quantitative PCR and bioinformatics methods. Methylation of the SNORA51 promoter in cancer and adjacent tissues was compared using bioinformatics. The relationship between SNORA51 expression levels and clinicopathological characteristics of patients with HCC, in addition to prognosis, was analyzed. The expression of SNORA51 in HCC was significantly higher compared with that in adjacent tissues (P<0.05). starBase demonstrated that higher expression levels of SNORA51 were associated with a significantly worse prognosis of patients with HCC compared with those who had lower expression levels of SNORA51 (P<0.05). Bioinformatics analysis using The University of Alabama at Birmingham Cancer Data Analysis Portal demonstrated that methylation of the SNORA51 promoter region in HCC was significantly decreased compared with adjacent tissues (P<0.05). A high expression of SNORA51 was significantly associated with portal vein tumor thrombus, vascular invasion and TNM stage (P<0.05). The median survival time of patients with high SNORA51 expression was significantly lower compared with those who had low SNORA51 expression (P<0.05). Both uni- and multivariate Cox regression analysis demonstrated that SNORA51 expression was an independent risk factor that significantly worsened the prognosis of patients with HCC (P<0.05). The overexpression of SNORA51 in patients with HCC was significantly associated with a poor prognosis and may be related to the reduced methylation of the SNORA51 promoter region. Therefore, SNORA51 may be a promising biomarker for prediction of the prognosis of patients with HCC and may be a therapeutic target for the treatment of HCC in future. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is an aging-related and heterogeneous hematopoietic malignancy. In this study, a total of 1,474 newly diagnosed AML patients with RNA sequencing data were enrolled, and targeted or whole exome sequencing data were obtained in 94% cases. The correlation of aging-related factors including age and clonal hematopoiesis (CH), gender, and genomic/transcriptomic profiles (gene fusions, genetic mutations, and gene expression networks or pathways) was systematically analyzed. Overall, AML patients aged 60 y and older showed an apparently dismal prognosis. Alongside age, the frequency of gene fusions defined in the World Health Organization classification decreased, while the positive rate of gene mutations, especially CH-related ones, increased. Additionally, the number of genetic mutations was higher in gene fusion--negative (GF-) patients than those with GF. Based on the status of CH- and myelodysplastic syndromes (MDS)-related mutations, three mutant subgroups were identified among the GF-AML cohort, namely, CH-AML, CH-MDS-AML, and other GF-AML. Notably, CH-MDS-AML demonstrated a predominance of elderly and male cases, cytopenia, and significantly adverse clinical outcomes. Besides, gene expression networks including HOXA/B, platelet factors, and inflammatory responses were most striking features associated with aging and poor prognosis in AML. Our work has thus unraveled the intricate regulatory circuitry of interactions among different age, gender, and molecular groups of AML. [ABSTRACT FROM AUTHOR]

This article discusses a study on gene editing in Salvia miltiorrhiza, a plant used in Eastern medicine to treat cardiovascular diseases. The researchers developed a protoplast regeneration system for S. miltiorrhiza using CRISPR/Cas9 gene editing technology. They targeted seven transcription factor genes involved in the production of bioactive compounds in the plant. The study demonstrated high-efficiency gene editing and the regeneration of knockout plants, which could potentially enhance the contents of active compounds in medicinal plants. [Extracted from the article]

Post-stroke depression (PSD) is a serious neuropsychiatric complication post stroke and leads to cognitive deficits. This study was conducted to explore the molecular mechanism of hypoxia-inducible factor-1α (HIF-1A) in cognitive dysfunction in rats with PSD. The rat model of PSD was established by middle cerebral artery occlusion, followed by 3 weeks of treatment with chronic unpredictable mild stress. The levels of miR-582–5p, HIF-1A, and neighbor of Brca1 gene (NBR1) in brain tissues were determined using RT-qPCR. The behaviors and cognitive capacity of rats were evaluated by various behavioral tests. PSD rats were injected with HIF-1A/miR-582–5p lowexpression vectors or NBR1 overexpression vectors via stereotactic method. The binding of HIF-1A to NBR1 or miR-582–5p was analyzed by chromatin immunoprecipitation and dual-luciferase assay. HIF-1A and NBR1 were highly expressed while miR-582–5p was poorly expressed in the brain of PSD rats. HIF-1A inhibition alleviated cognitive dysfunction of PSD rats. miR-582–5p was the upstream miRNA of HIF-1A, and HIF-1A specifically interacted with the NBR1 promoter to enhance NBR1 expression. miR-582–5p downregulation and NBR1 upregulation reversed the alleviative role of HIF-1A inhibition in cognitive dysfunction of PSD rats. In summary, HIF-1A inhibition may be a therapeutic target for cognitive dysfunction post PSD. [ABSTRACT FROM AUTHOR]