Overexpression of a Senescence-Related Gene CpSRG1 from Wintersweet (Chimonanthus praecox) Promoted Growth and Flowering, and Delayed Senescence in Transgenic Arabidopsis.

Plant senescence is a complex process that is controlled by developmental regulation and genetic programs. A senescence-related gene CpSRG1, which belongs to the 2OG-Fe(II) dioxygenase superfamily, was characterized from wintersweet, and the phylogenetic relationship of CpSRG1 with homologs from other species was investigated. The expression analysis by qRT-PCR (quantitative real-time PCR) indicated that CpSRG1 is abundant in flower organs, especially in petals and stamens, and the highest expression of CpSRG1 was detected in stage 6 (withering period). The expression patterns of the CpSRG1 gene were further confirmed in CpSRG1pro::GUS (ß-glucuronidase) plants, and the activity of the CpSRG1 promoter was enhanced by exogenous Eth (ethylene), SA (salicylic acid), and GA3 (gibberellin). Heterologous overexpression of CpSRG1 in Arabidopsis promoted growth and flowering, and delayed senescence. Moreover, the survival rates were significantly higher and the root lengths were significantly longer in the transgenic lines than in the wild-type plants, both under low nitrogen stress and GA3 treatment. This indicated that the CpSRG1 gene may promote the synthesis of assimilates in plants through the GA pathway, thereby improving growth and flowering, and delaying senescence in transgenic Arabidopsis. Our study has laid a satisfactory foundation for further analysis of senescence-related genes in wintersweet and wood plants. It also enriched our knowledge of the 2OG-Fe(II) dioxygenase superfamily, which plays a variety of important roles in plants.

Generation and Analysis of Expressed Sequence Tags from Chimonanthus praecox (Wintersweet) Flowers for Discovering Stress-Responsive and Floral Development-Related Genes.

A complementary DNA library was constructed from the flowers of Chimonanthus praecox, an ornamental perennial shrub blossoming in winter in China. Eight hundred sixty-seven high-quality expressed sequence tag sequences with an average read length of 673.8 bp were acquired. A nonredundant set of 479 unigenes, including 94 contigs and 385 singletons, was identified after the expressed sequence tags were clustered and assembled. BLAST analysis against the nonredundant protein database and nonredundant nucleotide database revealed that 405 unigenes shared significant homology with known genes. The homologous unigenes were categorized according to Gene Ontology hierarchies (biological, cellular, and molecular). By BLAST analysis and Gene Ontology annotation, 95 unigenes involved in stress and defense and 19 unigenes related to floral development were identified based on existing knowledge. Twelve genes, of which 9 were annotated as "cold response," were examined by real-time RT-PCR to understand the changes in expression patterns under cold stress and to validate the findings. Fourteen genes, including 11 genes related to floral development, were also detected by real-time RT-PCR to validate the expression patterns in the blooming process and in different tissues. This study provides a useful basis for the genomic analysis of C. praecox.

Morphine contributed to the deterioration of cancer via miR-543/MARCKS/FcγR-mediated phagocytosis pathway.

OBJECTIVES: It has been confirmed that morphine was detrimental to patients with cancers. Hence, we aimed to reveal a certain mechanism of morphine in cancer development. METHODS: Microarray and GSEA analysis were utilized to seek for differently expressed genes and pathway. KEY FINDINGS: Bioinformatics analysis identified that downregulation of MARCKS and upregulation of miR-543 in samples treated with morphine. FcγR-mediated phagocytosis pathway was illustrated to be upregulated in the control. PANC-1 and DU145 cell viability was increased but apoptosis was declined as morphine concentration went up from 10-8 to 10-6  mol/l. On the other curve, the viability was reduced and apoptosis was elevated from 10-6 to 10-5  mol/l. The expression of miR-543 ran the same trend as cell viability. Assays in vivo and in vitro validated that miR-543 facilitated cell viability, tumour growth, levels of CA199 and PSA, whereas inhibited apoptosis. MARCKS could target and inhibit miR-543 expression, which exhibited an opposite effect on cancer progression. MiR-543 blocked but MARCKS activated FcγR-mediated phagocytosis pathway. CONCLUSIONS: Morphine at 10-6  mol/l could benefit miR-543 expression to inhibit MARCKS expression, consequently, blocking FcγR-mediated phagocytosis pathway, which contributed to the cancer progression in vitro and in vivo.

Association between serum leptin levels and breast cancer risk: An updated systematic review and meta-analysis.

BACKGROUND: Many studies have indicated that leptin is correlated with breast cancer occurrence and tumor behavior. However, this issue remains controversial. Therefore, we conducted an updated meta-analysis to investigate the role of leptin in breast cancer. METHODS: We performed a systematic literature search and identified relevant papers up to 1 September 2017. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were used to evaluate effect sizes. RESULTS: Thirty-five eligible studies were included in the current meta-analysis. Serum leptin levels were related to breast cancer risk as demonstrated by calculations of the overall SMD = 0.46 (95% CI = 0.31-0.60, I = 93.5%). A subgroup analysis of BMI identified an association between breast cancer and serum leptin levels in patients who are overweight and obese (overweight: SMD = 0.35, 95% CI = 0.13-0.57, I = 88.1%; obesity: SMD = 1.38, 95% CI = 0.64-2.12, I = 89.6%). Additionally, menopausal status subgroup analysis revealed a significant association in postmenopausal women (SMD = 0.26, 95% CI = 0.12-0.40, I = 77.9%). Furthermore, we identified a significant association between breast cancer and serum leptin levels in Chinese women (SMD = 0.61, 95% CI = 0.44-0.79, I = 40.6%). CONCLUSION: The results of this meta-analysis suggested that leptin could be a potential biomarker for breast cancer risk in women, especially overweight/obese or postmenopausal women. Therefore, it may be useful for identifying subjects with a high risk for breast cancer who may benefit from preventive treatments.