Genomes of halophilic archaea typically contain multiple loci of integrated mobile genetic elements (MGEs). Despite the abundance of these elements, however, mechanisms underlying their site-specific integration and excision have not been investigated. Here, we identified and characterized a novel recombination system encoded by the temperate pleolipovirus SNJ2, which infects haloarchaeon Natrinema sp. J7-1. SNJ2 genome is inserted into the tRNAMet gene and flanked by 14 bp direct repeats corresponding to attachment core sites. We showed that SNJ2 encodes an integrase (IntSNJ2) that excises the proviral genome from its host cell chromosome, but requires two small accessory proteins, Orf2 and Orf3, for integration. These proteins were co-transcribed with IntSNJ2 to form an operon. Homology searches showed that IntSNJ2-type integrases are widespread in haloarchaeal genomes and are associated with various integrated MGEs. Importantly, we confirmed that SNJ2-like recombination systems are encoded by haloarchaea from three different genera and are critical for integration and excision. Finally, phylogenetic analysis suggested that IntSNJ2-type recombinases belong to a novel family of archaeal integrases distinct from previously characterized recombinases, including those from the archaeal SSV- and pNOB8-type families.
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths. Compound K, an active metabolite of ginsenosides, is reported to exhibit anti-cancer property in various types of human malignancies. The present study investigated the role of compound K on glucose metabolism in NSCLC cells and its underlying mechanism. Our study found that compound K dose-dependently inhibited the cell viability of NSCLC cells. Moreover, administration with compound K decreased glucose uptake and lactate secretion under normoxic and hypoxic conditions. Consistently, the expression of key enzymes (HK II, PDK1 and LDHA) involved in glucose metabolism were inhibited in compound K-treated tumor cells. In addition, compound K inhibited the expression of HIF-1α and its downstream gene GLUT1. On the contrary, overexpression of HIF-1α elevated metabolic reactions and partly attenuated the inhibitory role of compound K on NSCLC cell growth. These results demonstrate that compound K suppresses NSCLC cell growth via HIF-1α mediated metabolic alteration, contributing to novel anticancer therapy by targeting glucose metabolism.
Objective: Cell division cycle 25C (CDC25C) is involved in the regulation of the G2/M phase transition and is associated with various cancers, including non-small cell lung cancer. We evaluated its prognostic value in lung adenocarcinoma (LUAD) based on data from The Cancer Genome Atlas (TCGA).Methods: Kruskal-Wallis test, Wilcoxon signed-rank test, and logistic regression were used to evaluate relationships between clinical-pathologic features and CDC25C expression. Cox regression analyses and the Kaplan-Meier method were used to evaluate factors contributing to prognosis. Gene set enrichment analysis (GSEA) was performed.Results: High CDC25C expression in LUAD was associated with a high tumor extent (odds ratio (OR) = 2.23 (1.52-3.29), P < 0.001), regional lymph node invasion (OR = 2.18 (1.48-3.22), P < 0.001), OR = advanced stage (OR = 2.47 (1.72-3.59), P < 0.001), and poor status (OR = 1.87 (1.19-2.96), P = 0.007). A univariate analysis showed that high CDC25C expression is associated with a short overall survival (OS) (HR: 1.873; 95% CI: 1.385-2.535; P < 0.001) and poor progression-free survival (HR: 1.503; 95% CI: 1.173-1.926; P = 0.0012). In a multivariate analysis, high CDC25C expression was associated with poor OS (HR = 2.193; CI: 1.394-3.452, P = 0.001). GSEA showed the enrichment of cell cycle, apoptosis, p53-dependent G1 DNA damage response, S-phase, mitotic M-M G1 phases, and FA-mediated cell death in the CDC25C high-expression phenotype.Conclusions: CDC25C predicts poor prognosis in LUAD and may function in cell cycle regulation and FAS-mediated apoptosis.
This study aimed to systematically evaluate the value of combined detection of serum CEA and CA125 concentrations for the diagnosis of lung cancer.Related studies regarding the diagnosis of lung cancer were searched in PubMed, Embase, CNKI, and Wanfang using a computer. The number of patients who were true-positive, false-positive, false-negative, and true-negative were extracted from each study. Meta-analysis was performed using the Meta-Disc l.4, RevMan 5.3. Seven studies involving 2,216 cases were finally included. Regarding the diagnosis of lung cancer, the sensitivity, specificity, and diagnostic odds ratio of combined CEA and CA125 detection were higher than those of CEA detection alone. The area under the curve (AUC) of combined detection was 0.90, whereas the independently detected AUC was 0.73. Combined CEA and CA125 detection has higher diagnostic efficiency for lung cancer than CEA detection alone. The significance of combined serum CEA and CA125 detection in lung cancer is confirmed.
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