MicroRNA-383 inhibits anchorage-independent growth and induces cell cycle arrest of glioma cells by targeting CCND1

In recent years, microRNAs (miRNAs) have been proved to be closely related to the tumorigenesis and progression. An increasing number of researches have shown that microRNAs function as oncogenes or tumor suppressor genes in human malignant tumors. This study aims to explore the effects of microRNA-383 (miR-383) on malignant biological function of human gliomas. We detected the expression of miR-383 in glioma tissues and normal brain tissues by quantitative real-time PCR. Anchorage-independent growth assays, and flow cytometry were used to evaluate the functions of miR-383 that involves in cell growth and cell cycle. Western blotting assay was used to examine protein expression levels of Cyclin D1 (CCND1), a cell cycle-associated oncogene which has a predicted binding site of miR-383 within its 3′-untranslated region (3′-UTR), and luciferase activity assay was used to evaluate the 3′-UTR activity of CCND1. In this study, we found that miR-383 expression level was lower in gliomas than normal brain tissues. Overexpression of miR-383 in U251 and U87 cells showed a significant inhibitory effect on cell growth, which accompanied with cell cycle G0/G1 arrest as well as downregulation of CCND1 expression. Moreover, CCND1 was verified to be one of the direct targets of miR-383. In summary, this study suggested that miR-383 plays the role of tumor suppressor by targeting CCND1 in glioma cells, and may be useful for developing a new therapeutic strategy for gliomas.     

Syntheses and characterizations of a series of silver-carboxylate polymers

Self-assembly reaction of H₃btc (1,3,5-benzenetricarboxylic acid), H₂ta (1,4-benzenedicarboxylic acid) or 1,2,4,5-benzenetetracarboxylic dianhydride with Ag(NO₃) in mixed H₂O/MeOH solution at room temperature gave rise to four novel 3D polymeric silver(I) complexes, [{Ag(H₂btc)}{Ag₂(Hbtc)}]_n (1), [Ag(ta)_1/2]_n (2), [Ag₂(btec)_1/2]_n (3) and [{Ag₃(btec)_3/4}{Ag(H₂O)₂(btec)_1/4}]_n (4) (H₄btec=1,2,4,5-benzenetetracarboxylic acid). Complex 1 crystallizes in orthorhombic space group Fddd, with a=14.877(5), b=25.926(1), c=36.377(7) Å, Z=32. Complex 2 crystallizes in monoclinic space group P2₁/c, with a=7.257(6), b=8.949(8), c=6.346(5) Å, β=111.654(3)°, Z=4. Complex 3 crystallizes in orthorhombic space group P2₁/c, with a=8.333(8), b=6.335(5), c=10.964(9) Å, Z=4, whereas complex 4 crystallizes in triclinic space group , with a=7.509(1), b=9.351(1), c=10.307(7) Å, α=69.514(2), β=84.521(2), γ=83.638(2)°, Z=2. All compounds possess 3D framework and short Ag-Ag contacts are present in 1-4. In 1, the ligand unsupported Ag-Ag interactions play an important role in the formation of the complex, which is constructed by silver chains formed by Ag-Ag interactions and carboxylate spacers.     

Overexpression of CpSIZ1, a SIZ/PIAS-Type SUMO E3 Ligase from Wintersweet (Chimonanthus praecox), Delays Flowering,Accelerates Leaf Senescence and Enhances Cold Tolerance in Arabidopsis

Wintersweet (Chimonanthus praecox L.) is a traditional winter-flowering plant in China and a popular cut flower in winter. Its unique flowering characteristics under cold stress may involve the regulation of a large number of proteins. Protein post-translational modification is an important regulating type for the gene function. However, little is known about the post-translational modification in wintersweet. SUMOylation is an important post-translational modification in eukaryotes. Small ubiquitin-like modifier (SUMO) E3 ligases perform multiple functional regulatory activities in plants via SUMOylation. Here, we cloned and identified a SIZ/PIAS-type SUMO E3 ligase, CpSIZ1, from wintersweet. CpSIZ1 shared high similarity with other SIZ1 proteins. Quantitative real-time PCR (qRT-PCR) indicated that CpSIZ1 was expressed in all tissues tested, with the highest expression in flower wither period of stage 6, and followed by mature leaves except for different flower development stages. The ectopic expression of CpSIZ1 in Arabidopsis, including the CpSIZ1 overexpression in siz1-2 mutant (HB line) and CpSIZ1 overexpression in WT (OE line), not only promoted vegetative growth, delayed flowering and accelerated leaf senescence, but also improve the cold tolerance in Arabidopsis. Therefore, our studies have enrich the understanding of function of SIZ1 gene in woody plant, and provide a good foundation for further research on the post-translational modification regulation mechanism in this winter-flowering plant.

     

海产品嗜冷菌波罗的海希瓦氏菌中3个冷激蛋白功能分析

【目的】波罗的海希瓦氏菌是冷藏海产品中常见的腐败菌,而该菌中关于冷激蛋白的功能研究尚未见报道。本研究从分子生物学角度分析波罗的海希瓦氏菌中3个冷激蛋白各自的功能。【方法】采用BEAST软件分析γ-变形菌纲中部分食源性微生物的冷激蛋白进化时间,接着利用实时荧光定量PCR方法检测波罗的海希瓦氏菌3个冷激蛋白基因的表达规律,进而构建3个冷激蛋白的基因敲除株,分析敲除株在不同温度和不同环境胁迫条件下的生长状况、群体感应现象以及致腐能力,最后构建3个冷激蛋白的异源表达菌株并分析它们在不同温度和不同环境胁迫条件下的生长状况。【结果】波罗的海希瓦氏菌中鉴定到3个冷激蛋白,分别为cspC、cspD、cspG。所有γ-变形菌纲的cspD基因单独聚成一支,并于1 109.6百万年前与其他csp基因相分离,波罗的海希瓦氏菌的cspC和cspG在858.8百万年前互相分开。cspG基因是波罗的海希瓦氏菌低温生存的必需基因,且广泛响应环境胁迫条件;cspC基因对cspG基因功能的实施起辅助作用;cspD不响应冷激,但却会随生长阶段的变化而发生变化。此外,cspC基因和cspG基因在低温条件下与细菌的致腐能力相关。【结论】波罗的海希瓦氏菌3个冷激蛋白基因各有不同,且cspC基因和cspG基因与该菌致腐能力有关,这为今后研究腐败菌的冷适应和致腐机制提供了新思路。     

Knockdown of Burton’s tyrosine kinase confers potent protection against sepsis-induced acute lung injury

Sepsis is a common and critical complication in surgical patients that often leads to multiple organ failure syndrome (MOFS), including acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Despite intensive supportive care and treatment modalities, the mortality of these patients remains high. In this study, we investigated the role of Burton’s tyrosine kinase (BTK), a member of the Btk/Tec family of cytoplasmic tyrosine kinases, in the pathogenesis of sepsis, and evaluated the protective effect of in vivo Btk RNA interference in a mouse model of cecal ligation and puncture (CLP)-induced sepsis. After intratracheal injection of Btk siRNA, the mice were then subjected to CLP to induce sepsis. The results demonstrated that this approach conferred potent protection against sepsis-induced ALI, as evidenced by a significant reduction in pathological scores, epithelial cell apoptosis, pulmonary edema, vascular permeability, and the expression of inflammatory cytokines and neutrophil infiltration in the lung tissues of septic mice. In addition, RNA interference of Btk significantly suppressed p-38 and iNOS signaling pathways in transduced alveolar macrophages in vitro. These results identify a novel role for BTK in lethal sepsis and provide a potential new therapeutic approach to sepsis and ALI.