Phylogenetic analysis of achaete-scute complex genes in metazoans.

Achaete-scute complex (ASC) genes play essential roles in regulating neurogenesis of metazoans. Various metazoan species have greatly different numbers of genes in ASCa, ASCb and ASCc families. To explore evolutionary mechanisms of metazoan ASC genes, Blast (basic local alignment search tool) searches and phylogenetic analyses were conducted to identify ASC genes in metazoan species and to infer phylogenetic relationship between various ASC genes. As a result, 2784 ASC genes were identified in 804 metazoan species. The phylogenetic tree constructed using 1237 unique bHLH motifs shows that metazoan ASCa, ASCb and ASCc families contain six (a1-a6), five (b1-b5) and three (c1-c3) bHLH genes, respectively. Further phylogenetic analyses suggest that ASC genes in metazoans are derived from a primitive c gene, those in insects are derived from c2 gene, and those in chordates are derived from a2 and a3 genes. Data of gene linkage demonstrate that insect a6 is derived from a4 but not from a5, and chordate a2 is ancestral to b5 only, whilst a3 is ancestral to both b3 and b5. It is concluded that current ASC gene families in metazoans were established through a series of sub- and/or neo-functionalization to duplicated ancestral ASC gene(s). These results provide good references for exploring evolutionary mechanisms of other bHLH genes in metazoans. Besides, gene subtyping is considered as an efficient method for evolutionary studies on closely related homologous genes.

Prevalence of sarcopenic obesity in patients with diabetes and adverse outcomes: A systematic review and meta-analysis.

BACKGROUND & AIMS: Sarcopenic obesity (SO), which refers to the coexistence of sarcopenia and obesity. The aim of this systematic review and meta-analysis was first to assess the prevalence of SO in patients with diabetes, and second, to evaluate possible adverse outcomes. METHODS: This study was conducted in adherence to the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines and the data were collated by means of meta-analysis and narrative synthesis. We comprehensively and systematically searched PubMed, Embase, Web of Science, CBM, CNKI, Wanfang Database from the establishment of the database to December 2022, and collected related studies on SO in patients with diabetes. Using Stata 16.0 software to pool the estimates for the prevalence of SO in patients with diabetes, and a descriptive systematic review of possible adverse outcomes was performed. RESULTS: The prevalence of 20 included studies were pooled by a random-effects model, which showed that the prevalence of SO in patients with diabetes was 27%. Subgroup analyses showed that the prevalence of SO was higher among studies using BIA (24%) to assess muscle mass, and those focused on literature of moderate-quality (29%), being published from 2013 to 2016 (29%), female patients with diabetes (17%), North Americans (30%). SO in patients with diabetes can lead to adverse outcomes including decreased glomerular filtration rate, massive proteinuria, cognitive decline, and insulin resistance. CONCLUSION: The systematic review and meta-analysis revealed a prevalence of 27% for SO in patients with diabetes, and it is associated with potential serious adverse outcomes. Therefore, we should attach importance to the screening of SO in patients with diabetes and early detection of susceptible groups, then selecting appropriate interventions to reduce the occurrence of it and various adverse outcomes in this demographic.

Human SARS-CoV-2 has evolved to reduce CG dinucleotide in its open reading frames.

The outbreak of COVID-19 has brought great threat to human health. Its causative agent is a severe acute respiratory syndrome-related coronavirus which has been officially named SARS-CoV-2. Here we report the discovery of extremely low CG abundance in its open reading frames. We found that CG reduction in SARS-CoV-2 is achieved mainly through mutating C/G into A/T, and CG is the best target for mutation. Meanwhile, 5'-untranslated region of SARS-CoV-2 has high CG content and is capable of forming an internal ribosome entry site (IRES) to recruit host ribosome for translating its RNA. These features allow SARS-CoV-2 to reproduce efficiently in host cells, because less energy is consumed in disrupting the stem-loops formed by its genomic RNA. Notably, genomes of cellular organisms also have very low CG abundance, suggesting that mutating C/G into A/T occurs universally in all life forms. Moreover, CG is the dinucleotide related to CpG island, mutational hotspot and single nucleotide polymorphism in cellular organisms. The relationship between these features is worthy of further investigations.

Non-coding RNA 886 promotes renal cell carcinoma growth and metastasis through the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway.

Non-coding RNA 886 (nc886) has been suggested to serve tumor-suppressing roles in several cancer cells. However, the expression pattern of nc886 and its function in renal cell carcinoma (RCC) has not been reported until now. The present study aimed to examine the expression of nc886 in human RCC tissues and to investigate the role of nc886 in RCC cell proliferation, apoptosis and invasion in vitro. Furthermore, whether nc886 exerts its function on RCC via Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling was investigated. It was demonstrated that nc886 is overexpressed in human RCC tissues compared with normal tissues, as determined by reverse transcription-quantitative polymerase chain reaction analysis. The nc886 mimic and inhibitor were transfected into the A­498 cells to overexpress or knock down nc886 expression. Cell proliferation, cell apoptosis rate and cell invasion ability were determined by MTT, flow cytometry and Transwell­Matrigel invasion assays. The results demonstrated that nc886 overexpression promotes A­498 cell proliferation and invasion, and inhibits cell apoptosis, while nc886 knockdown resulted in the opposite effects. Furthermore, nc886 could activate the JAK2/STAT3 signaling pathway in A­498 cells. AG490, an inhibitor of JAK2, could attenuate the effects of nc886 on cell proliferation, apoptosis and invasion. In conclusion, to the best of our knowledge, the present study for the first time revealed the expression profile and the tumor­promoting role of nc886 in RCC. nc886 affects RCC cell proliferation, apoptosis and invasion at least partially via the activation of JAK2/STAT3 signaling. This study may provide a useful therapeutic target for RCC.