胃癌组织长链非编码RNA ZDHHC8P1、MEG3、TUG1表达与临床病理特征及预后的关系研究

目的:探讨胃癌组织长链非编码RNA(lncRNA)DHHC型锌指蛋白8假基因1(ZDHHC8P1)、母系表达基因3(MEG3)、牛磺酸上调基因1(TUG1)表达与临床病理特征和预后的关系。方法:选取2013年1月至2016年1月我院病理科收集的83例胃癌患者经手术切除或胃镜活检的癌组织及癌旁组织石蜡标本,检测胃癌和癌旁组织中ZDHHC8P1、MEG3、TUG1表达。分析ZDHHC8P1、MEG3、TUG1表达与胃癌临床病理特征的关系。随访所有患者,分析ZDHHC8P1、MEG3、TUG1表达与患者预后的关系。结果:胃癌组织中ZDHHC8P1、TUG1表达量均高于癌旁组织(P0.05),MEG3表达量低于癌旁组织(P0.05)。ZDHHC8P1表达与肿瘤直径、分化程度、浸润深度、TNM分期、淋巴结转移、远处转移有关(P0.05),MEG3、TUG1表达与分化程度、浸润深度、淋巴结转移有关(P0.05)。Kaplan-Meier生存曲线分析结果显示ZDHHC8P1、TUG1高表达患者无疾病进展生存(PFS)率、总生存(OS)率低于ZDHHC8P1、TUG1低表达患者(P0.05),MEG3低表达患者PFS、OS率低于MEG3高表达患者(P0.05)。Cox风险回归分析结果显示淋巴结转移、ZDHHC8P1高表达、TUG1高表达、MEG3低表达是胃癌患者不良预后的危险因素(HR=1.613、1.956、2.512、-0.824,P0.05)。结论:胃癌组织中ZDHHC8P1、TUG1呈高表达,MEG3呈低表达,ZDHHC8P1、TUG1、MEG3表达均与胃癌临床病理特征和预后有关,可作为胃癌患者预后评估的辅助指标。     

Could urinary ACE2 protein level help identify individuals susceptible to SARS-CoV-2 infection and complication?

Science China Life Sciences -     

全反式维甲酸对骺软骨细胞生物学行为及其功能影响的研究

该研究主要探讨了体外高浓度全反式维甲酸(all-trans retinoic acid,ATRA)对SD大鼠骺软骨细胞生物学性状和功能的影响以及体内ATRA对SD大鼠胫骨生长板的影响。以SD大鼠骺软骨细胞为研究对象、ATRA为干预因素,采用CCK-8、细胞流式术、HE染色、Annexin V-FITC细胞凋亡流式检测术、Hoechst染色、细胞划痕、Transwell实验分别评估ATRA处理后细胞的增殖、周期、形态、凋亡及迁移情况,Western blot检测蛋白聚糖、Ⅱ型胶原、X型胶原等相关功能蛋白的变化;以3周雄性SD大鼠为实验对象,分为对照组、60 mg/kg·d ATRA组、80 mg/kg·d ATRA组,进行10天连续ATRA灌胃处理,测量每只SD大鼠灌胃第1天、第10天的头尾长,处理10天后对胫骨生长板进行HE染色。结果表明,ATRA作用SD大鼠骺软骨细胞后,增殖能力减弱且细胞周期被阻滞在S期(P<0.01),细胞形态由三角形、多边形变为长条状,凋亡的发生增多(P<0.01),迁移能力受到抑制(P<0.05)以及Western blot结果显示蛋白聚糖、Ⅱ型胶原、X型胶原等功能相关蛋白较对照组表达均明显降低(P<0.01);对SD大鼠进行ATRA灌胃处理后,与对照组比较,60 mg/kg·d ATRA组和80 mg/kg·d ATRA组的头尾长均变短(P<0.01);胫骨生长板HE染色显示,ATRA灌胃组的生长板变窄甚至闭合。该研究证实了体外高浓度ATRA能够对SD大鼠骺软骨细胞的增殖、迁移起抑制作用,同时能够诱导凋亡,降低相关功能蛋白的表达,在SD大鼠体内证实,过量ATRA可影响生长板软骨内成骨过程,最终使生长板部分或全部提前闭合,进而影响SD大鼠身长的增长。     

GPI7-mediated glycosylphosphatidylinositol anchoring regulates appressorial penetration and immune evasion during infection of Magnaporthe oryzae

Glycosylphosphatidylinositol (GPI) anchoring plays key roles in many biological processes by targeting proteins to the cell wall; however, its roles are largely unknown in plant pathogenic fungi. Here, we reveal the roles of the GPI anchoring in Magnaporthe oryzae during plant infection. The GPI-anchored proteins were found to highly accumulate in appressoria and invasive hyphae. Disruption of GPI7, a GPI anchor-pathway gene, led to a significant reduction in virulence. The Δgpi7 mutant showed significant defects in penetration and invasive growth. This mutant also displayed defects of the cell wall architecture, suggesting GPI7 is required for cell wall biogenesis. Removal of GPI-anchored proteins in the wild-type strain by hydrofluoric acid (HF) pyridine treatment exposed both the chitin and β-1,3-glucans to the host immune system. Exposure of the chitin and β-1,3-glucans was also observed in the Δgpi7 mutant, indicating GPI-anchored proteins are required for immune evasion. The GPI anchoring can regulate subcellular localization of the Gel proteins in the cell wall for appressorial penetration and abundance of which for invasive growth. Our results indicate the GPI anchoring facilitates the penetration of M. oryzae into host cells by affecting the cell wall integrity and the evasion of host immune recognition.     

NbALY916 is involved in potato virus X P25-triggered cell death in Nicotiana benthamiana

Systemic necrosis often occurs during viral infection of plants and is thought mainly to be the result of long-term stress induced by viral infection. Potato virus X (PVX) encodes the P25 pathogenicity factor that triggers a necrotic reaction during PVX-potato virus Ysynergistic coinfection. In this study, we discovered that NbALY916, a multifunctional nuclear protein, could interact with P25. When NbALY916 expression was reduced by tobacco rattle virus (TRV)-based virus-induced gene silencing, the accumulation of P25 was increased, which would be expected to cause more severe necrosis. However, silencing of NbALY916 reduced the extent of cell death caused by P25. Furthermore, we found that overexpression of NbALY916 increased the accumulation of H₂O₂ and triggered more extensive cell death when coexpressed with P25, even though accumulation of P25 was itself reduced by the increased expression of NbALY916. Furthermore, transient expression of P25 specifically induced the expression of NbALY916 mRNA, but not the mRNAs of three other ALYs in Nicotiana benthamiana. In addition, we showed that silencing of NbALY916 or transient overexpression of NbALY916 affected the infection of PVX in N. benthamiana. Our results reveal that NbALY916 has an antiviral role that, in the case of PVX, operates by inducing the accumulation of H₂O₂ and mediating the degradation of P25.