KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p

Nonsmall cell lung cancer (NSCLC) is one of the leading causes of cancer‐related death worldwide. Kinesin family member 2C (KIF2C), a modulator in microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to take roles in cancer biology, but its role in NSCLC remains unclear. This study was intended to investigate the expression and function of KIF2C in NSCLC. Our results demonstrated that KIF2C was up‐regulated in NSCLC tissues and cell lines. The high expression of KIF2C in NSCLC tissues was significantly correlated with higher T stage (0.0078), worse differentiation status (0.0049), and lymph node metastasis (P < .0001). We also proved that the high expression level of KIF2C predicted worse prognosis of the patients. After knockdown of KIF2C, the proliferation and metastasis of NSCLC cells were inhibited. Luciferase reporter assay suggested that KIF2C was a target gene of miR‐325‐3p, which was reported to be a tumour suppressor in NSCLC. In conclusion, this study proved an oncogenic role of KIF2C in NSCLC and partly clarified the mechanism of its high expression. Our findings provided a useful insight into the mechanism of NSCLC progression and offered clues to novel therapy strategies.     

Retracted: microRNA-129-5p involved in the neuroprotective effect of dexmedetomidine on hypoxic-ischemic brain injury by targeting COL3A1 through the Wnt/β-catenin signaling pathway in neonatal rats

Our study aims to elucidate the mechanisms how microRNA-129-5p (miR-129-5p) involved in the neuroprotective effect of dexmedetomidine (DEX) on hypoxic-ischemic brain injury (HIBI) by targeting the type III procollagen gene (COL3A1) through the Wnt/β-catenin signaling pathway in neonatal rats. A total of 120 rats were obtained, among which 15 rats were selected as sham group and rest rats as model, DEX, DEX + negative control (DEX + NC), DEX + miR-129-5p mimics, DEX + miR-129-5p inhibitors, DEX + XAV-939, and DEX + miR-129-5p inhibitors + XAV-939 groups. A dual-luciferase reporter assay was performed for the target relationship between miR-129-5p and COL3A1. Weight rate and water content of cerebral hemisphere were detected. Quantitative real-time polymerase chain reaction and Western blot analysis were conducted to detect miR-129-5p expression and expressions of COL3A1, E-cadherin, T-cell factor (TCF)− 4, and β-catenin. The DEX, DEX + miR-129-5p mimics, DEX + XAV-939 groups had increased weight rate of the cerebral hemisphere, but decreased water content of left cerebral hemisphere, levels of COL3A1, β-catenin, TCF-4, and E-cadherin in the hippocampus compared with the model and DEX + miR-129-5p inhibitors groups. COL3A1 was verified as the target gene of the miR-129-5p. Compared with the DEX + NC and DEX + miR-129-5p inhibitors + XAV-939 groups, the DEX + XAV-939 and DEX + miR-129-5p mimics groups had elevated weight rate of the cerebral hemisphere, but reduced water content of left cerebral hemisphere, levels of COL3A1, β-catenin, TCF-4, and E-cadherin in the hippocampus. Our findings demonstrate that miR-129-5p improves the neuroprotective role of DEX in HIBI by targeting COL3A1 through the Wnt/β-catenin signaling pathway in neonatal rats.     

(+)-12alpha-Hydroxysophocarpine, a new quinolizidine alkaloid and related anti-HBV alkaloids from Sophora flavescens

(+)-12alpha-Hydroxysophocarpine (8), a new quinolizidine alkaloid was isolated from the roots of Sophora flavescens, together with 10 known quinolizidine alkaloids, (+)-oxymatrine (1), (+)-matrine (2), (+)-9alpha-hydroxymatrine (3), (+)-allomatrine (4), (+)-oxysophocarpine (5), (-)-sophocarpine (6), (-)-9alpha-hydroxysophocarpine (7), (+)-lehmannine (9), (-)-13,14-dehydrosophoridine (10), and (-)-anagyrine (11). Their structures were elucidated by spectroscopic methods, and the stereochemistry of 8 was confirmed by X-ray analysis. These alkaloids were tested for anti-hepatitis B virus (HBV) activity in vitro, compounds 5, 6, 9, and 10 showed significant anti-HBV activity with inhibitory potency against HBsAg secretion at 48.3-79.3% and that against HBeAg secretion at 24.6-34.6%.     

Role of methylenetetrahydrofolate reductase 677C→T polymorphism in the development of myocardial infarction: evidence from an original study and updated meta-analysis

The methylenetetrahydrofolate reductase (MTHFR) gene variant 677C→T is considered a risk factor for myocardial infarction (MI) in Caucasians, but it remains unclear whether this applies to Chinese or other Asian populations. A total of 551 controls and 304 age-matched Chinese MI patients were recruited. MTHFR genotypes were determined. A subsequent meta-analysis was performed to determine the association between MTHFR and MI in Asia. Conventional risk factors such as hypertension, diabetes mellitus and low-density lipoprotein exhibited no significant differences between the two groups. Genotype frequencies among cases and controls were compatible with Hardy–Weinberg equilibrium. The frequencies of CC, CT and TT genotypes were 28, 46 and 26 % for patients with MI and 31, 52 and 17 % for the matched control group (p = 0.006). T-allele frequency in MI patients was higher than in controls (49 vs. 43 %, odds ratio = 0.785, 95 % confidence interval = 0.644–0.958, p = 0.017). A total of 16 studies including ours were identified, involving 4053 patients and 6791 controls. A recessive genotype model of MTHFR 677C→T polymorphism, but not a dominant genotype model, was significantly associated with greater MI risk in Asians. MI risk increased 48, 37 and 47 % for the TT homozygote compared with the CC wild type, CT heterozygote and the combination of CT and CC. Thus, we conclude that the MTHFR gene variant 677C→T is a risk factor for MI in the Chinese population and the TT genotype is associated with a significant increase in MI risk in Asia.     

人促甲状腺素受体膜外区蛋白在原核系统表达及其生物活性鉴定

为研究重组人促甲状腺素受体 (hTSHR)膜外区表达产物及其生物活性与免疫活性 ,将hT SHR膜外区编码基因 (编码第 3～ 4 2 0位氨基酸 )重组到表达型质粒pGEX 4T 3上 ,测序结果表明序列正确 ,未改变读码框架 .然后转入E .coliAd4 94进行诱导表达 .纯化后的表达产物经SDS PAGE、Western印迹及放射受体法分别检测其分子量、免疫活性和生物活性 .重组TSHR3～ 4 2 0 膜外区蛋白 (简称TSHR3～ 4 2 0 )产率为 15 9～ 2 0 2 μg L培养基 ,分子量为 4 8.9kD ;融合蛋白 (简称GST TSHR3～ 4 2 0 )分子量为 75 .4kD .两种表达产物都可与TSHRAb反应 ;TSHR3～ 4 2 0 可与12 5I TSH结合 .     

Improvement of industry-applied rifamycin B-producing strain,Amycolatopsis mediterranei,by rational screening

An industrially applied rifamycin B-producing strain, Amycolatopsis mediterranei XC 1-02, was used for further screening. A special mutation and screening procedure was adopted to select a strain, which can alleviate the inhibition caused by both aromatic amino acid and p-hydroxybenzoic acid in the pathway of rifamycin B biosynthesis as well as enhance the production of propionate, one of the precursors of rifamycin B biosynthesis. By the above methods, a strain A. mediterranei XC 9-25 was obtained, and its rifamycin B productivity in shaking flask reaches 10 g/L, which is 2.38 times higher than that of the ancestral strain XC 1-02. The productivity of rifamycin B fed-batch fermentation in 60000 L fermentor with A. mediterranei XC 9-25 reached 19.11 g/L.     

禽Ⅰ型副粘病毒f基因克隆及序列分析

用RT-PCR一步法对云南省不同禽类(鸡、鸽子)3株禽I型副粘病毒F基因进行扩增和克隆,并对其f基因片段核苷酸序列进行分析,结果表明,云南省禽I型副粘病毒各毒株同源性为88.1%～94.9%,与疫苗株LaSota和强毒株F48E9的同源性为85.6%.所分离两株新城疫病毒在F蛋白裂解位点区(112～117aa)的氨基酸序列与强毒株在这一区域的序列完全相同,表明为强毒株.鸽I型副粘病毒F蛋白裂解位点区的氨基酸序列与PPMV ZQ98-1株在这一区域的序列完全相同,揭示为中强毒株.以1 662bp核苷酸绘制系统发育树,表明云南地方新城疫病毒属于基因Ⅶ型,鸽I型副粘病毒属于基因Ⅵ型.