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| 1 | MicroRNA-124 mediates the cholinergic anti-inflammatory action through inhibiting the production of pro-inflammatory cytokines显示文摘迷走神经神经能通过“一条胆碱能的反煽动性的小径”控制煽动性的反应,它被 α 调停; 7-nicotinic 醋胆素受体(α 7nAChR ) 在巨噬细胞上。然而,连接 α 的细胞内部的机制; 7nAChR 激活和支持 inflammatory cytokine 生产遗体不好理解。在这研究,我们发现 miR-124 是由在暴露 LPS 的房间和老鼠的胆碱能的收缩筋的 upregulated。利用 miR-124 模仿并且 siRNA 击倒,我们证明 miR-124 是为胆碱能的反煽动性的行动的一个批评调停人。而且,我们的数据显示 miR-124 由指向信号变换器和抄写 3 的使活跃之物(STAT3 ) 到减少 IL-6 生产和 TNF-α 调制导致 LPS 的 cytokine 生产;变换酶(不作声) 减少 TNF-α版本。这些结果也显示 miR-124 是为煽动性的疾病的处理的一个潜在的治疗学的目标。 | Yang Sun Qi Li Huan Gui Dong-Ping Xu Yi-LiYang Ding-Feng Su Xia Liu | 2013 | Cell Research2013，23，11： | 35 |
| 2 | MIWI and piRNA-mediated cleavage of messenger RNAs in mouse testes显示文摘piRNA 机械在调停以它的角色著名 transposons 的 epigenetic silencing。最近的研究建议这功能也包含导出 transposon 的抄本的指导 piRNA 的劈开。同样多 piRNAs 也看起来有能力指向多样的 mRNAs,这提起 piRNAs 可以与 siRNAs 比广泛地扮演降级的吸引人的可能性特定的 mRNAs。直接测试这个假设,我们比较了联系的老鼠 PIWI (MIWI ) 有从老鼠睾丸的试验性地识别的劈开的 mRNA 碎片的 piRNAs,和主要发生在的观察劈开地点从 5 ′ 放 10;通常认为的指向结束 piRNAs。我们也注意了强壮的偏爱因为分别地,在核苷酸的 U 和 A 残余在 piRNAs 和 mRNA 碎片放 1 和 10,由“乒乓球”类似于 piRNA 扩大的模式的特征骑车。通过由介绍的 CLIP-seq 和基因表示 MIWI-RNA 相互作用印射,我们发现许多潜在的指向 piRNA 的 mRNAs 直接与 MIWI 交往,表演在 Miwi 的睾丸提高了表达式层次催化变异的鼠标。基于记者的试金进一步揭示了在调停 piRNA 的目标压抑的为 slicer 活动和 MIWI 的装载 piRNA 能力的在 piRNAs 和 mRNA 目标和要求之间的基础配对的重要性。重要地,我们证明某些关键 piRNA 目标的那合适的周转为精子形成是必要的。一起,这些调查结果为男细菌房间开发和成熟在鼠标睾丸和它的中央要求揭示 piRNA 机械的象 siRNA 一样函数。 | Peng Zhang Jun-Yan Kang Lan-Tao GOU Jiajia Wang Yuanchao Xue Geir Skogerboe Peng Dai Da-Wei Huang Runsheng Chen Xiang-Dong Fu Mo-Fang Liu Shunmin He | 2015 | Cell Research2015，25，2： | 35 |
| 3 | 靶向siRNA阻断Wnt/β-catenin信号通路对子宫内膜异位症患者在位子宫内膜基质细胞VEGF、MMP-9表达的影响显示文摘目的通过观察人子宫内膜异位症在位子宫内膜基质细胞β-catenin的表达,及利用siRNA靶向沉默β-catenin基因以阻断Wnt/β-catenin信号通路来观察其下游靶基因血管内皮生长因子(vascular endothelial growth factor,VEGF)和基质金属蛋白酶-9(matrix metalloproteinases-9,MMP-9)表达的变化,探讨Wnt/β-catenin信号通路在子宫内膜异位症发生机制中的作用。方法采用随机、对照设计,将体外分离、培养的24例子宫内膜异位症患者在位子宫内膜基质细胞分成3组(n=8):空白组、阴性组(以含阴性荧光siRNA 100pmol和转染试剂5μg的混合物转染)以及siRNA干扰组(以含β-catenin siRNA 100pmol和转染试剂5μg的混合物转染),并以10例非子宫内膜异位症患者子宫内膜基质细胞作为正常组。利用Real-time PCR和Western blot方法分别检测子宫内膜异位症在位子宫内膜空白组和非子宫内膜异位症正常组β-catenin的表达。转染24h后,用以上方法分别检测子宫内膜异位症空白组、阴性组和siRNA干扰组β-catenin、VEGF以及MMP-9的表达。结果子宫内膜异位症空白组β-catenin mRNA和蛋白的表达明显高于非子宫内膜异位症正常组(均P<0.05)。子宫内膜异位症siRNA干扰组β-catenin、VEGF以及MMP-9mRNA和蛋白的表达明显低于空白组和阴性组(均P<0.05),而空白组与阴性组之间差异无统计学意义(均P>0.05)。结论子宫内膜异位症在位子宫内膜基质细胞β-catenin的表达明显高于非子宫内膜异位症患者,阻断Wnt/β-catenin信号通路后,其下游靶基因VEGF、MMP-9的表达明显受到抑制。因此,Wnt/β-catenin信号通路可能在子宫内膜异位症的发生机制中起重要作用。 | 刘儒彪 刘义 于岚 郑婷婷 王罡 | 2016 | 华中科技大学学报(医学版)2016，45，1： | 29 |
| 4 | microRNA研究进展显示文摘小分子RNA家族中的一员——microRNA,是一段非常短的非编码RNA序列,对多种生物学过程起调控作用。本文试从microRNA的结构特点、合成及作用机制和功能等方面对microRNA的研究进展作一个简单回顾。 | 华友佳 肖华胜 | 2005 | 生命科学2005，17，3： | 27 |
| 5 | MicroRNA-221 inhibits CDKNIC/p57 expression in human colorectal carcinoma显示文摘 | Kai SUN Wei WANG Jun-jie ZENG Cheng-tang WU Shang-tong LEI Guo-xin LI | 2011 | Acta Pharmacologica Sinica2011，32，3： | 27 |
| 6 | siRNA therapeutics:a clinical reality显示文摘Since the revolutionary discovery of RNA interference(RNAi),a remarkable progress has been achieved in understanding and harnessing gene silencing mechanism;especially in small interfering RNA(siRNA)therapeutics.Despite its tremendous potential benefits,major challenges in most siRNA therapeutics remains unchanged-safe,efficient and target oriented delivery of siRNA.Twenty years after the discovery of RNAi,siRNA therapeutics finally charts its way into clinics.As we journey through the decades,we reminisce the history of siRNA discovery and its application in a myriad of disease treatments.Herein,we highlight the breakthroughs in si RNA therapeutics,with special feature on the first FDA approved RNAi therapeutics Onpattro(Patisiran)and the consideration of effective siRNA delivery system focusing on current siRNA nanocarrier in clinical trials.Lastly,we present some challenges and multiple barriers that are yet to be fully overcome in siRNA therapeutics. | Phei Er Saw Er-Wei Song | 2020 | Science China(Life Sciences)2020，63，4： | 26 |
| 7 | Inhibition of STAT3 expression by siRNA suppresses growth and induces apoptosis in laryngeal cancer cells显示文摘Aim: To determine the inhibitory effect of the synthetic STAT3 siRNA on the expression of STAT3 gene in human laryngeal cancer cell lines Hep2 and to investigate the effect of STAT3 siRNA on growth and apoptosis in Hep2 cells. Methods: A pair of DNA templates coding siRNA against STAT3-mRNA was synthesized to reconstruct plasmid of pSilencer1.0-U6 siRNA-STAT3. Hep2 cells were transfected with RPMI-1640 media (untreated), plasmid (empty), and STAT3 siRNA, respectively. Northern blot and Western blot analysis of STAT3 and pTyr-STAT3 expression in Hep2 cells and Western blot analysis of Bcl-2 expression in the Hep2 cell was performed 72 h after transfection. MTT, flow cytometry, and AO/EB assay were used for determination of cells proliferation and apoptosis in Hep2 cells. Results: pTyr-STAT3 was markedly expressed in untreated Hep2 cells and the vector-treated Hep2 cells, whereas pTyr-STAT3 expression was significantly reduced in STAT3 siRNA-transfected Hep2 cells, indicating that STAT3 siRNA inhibited the activity of STAT3. Transfection of Hep2 cells with STAT3 siRNA significantly inhibited STAT3 expression at both mRNA and protein level in Hep2 cells and the inhibition was characterized by time-dependent transfection. Treatment of Hep2 cells with STAT3 siRNA resulted in dose-dependent growth inhibition of Hep2, this significantly increased apoptotic cell rate, and decreased Bcl-2 expression level in Hep2 cells. STAT3 siRNA had an effect on induction of either early or late stage apoptosis. Conclusion: This study demonstrates that STAT3 siRNA effectively inhibits STAT3 gene expression in Hep2 cells leading to growth suppression and induction of apoptosis in Hep2 cells. The use of siRNA technique may provide a novel therapeutic approach to treat laryngeal cancer and other malignant tumors expressing constitutively activated STAT3. | Li-fangGAO De-qiXU Lian-jiWEN Xing-yiZHANG Yue-tingSHAO Xue-jianZHAO | 2005 | Acta Pharmacologica Sinica2005，26，3： | 24 |
| 8 | Reversal of the phenotype by K-ras^(val12) silencing mediated by adenovirus-delivered siRNA in human pancreatic cancer cell line Panc-1显示文摘AIM: To investigate the in vitro antitumor effect of adenovirus-mediated small interfering RNAs (siRNAs) on pancreatic cancer and the associated mechanism.METHODS: A 63-nucleotide (nt) oligonucleotide encoding K-ras^val12 and specific siRNA were introduced into pSilencer 3.1-H1, then the H1-RNA promoter and siRNA coding insert were subcloned into pAdTrack to get plasmid pAdTrackH1-K-ras^val12. After homologous recombination in bacteria and transfections of such plasmids into a mammalian packaging cell line 293, siRNA expressing adenovirus AdH1-K-ras^val12 was obtained. Stable suppression of K-ras^val2 was detected by Northern blot and Western blot. Apoptosis in Panc-1 cells was detected by flow cytometry.RESULTS: We obtained adenovirus AdH1-K-ras^val12 carrying the pSilencer 3.1-H1 cassette, which could mediate gene silencing. Through siRNA targeted K-ras^val12, the oncogenic phenotype of cancer cells was reversed. Flow cytometry showed that apoptotic index of Panc-1 cells was significantly higher in the AdH1-K-ras^val12-treatment group (18.70% at 72 h post-infection, 49.55% at 96 h post-infection)compared to the control groups (3.47%, 3.98% at 72 and 96 h post-infection of AdHl-empty, respectively, 4.21%,3.78% at 72 and 96 h post-infection of AdH1-p53,respectively) (P<0.05).CONCLUSION: These results demonstrate that adenoviral vectors can be used to mediate RNA interference (RNAi)to induce persistent loss of functional phenotypes. In gene therapy, the selective down-regulation of only the mutant version of a gene allows for highly specific effects on tumor cells, while leaving the normal cells untouched. In addition, the apoptosis of pancreatic cancer cell line Panc-1 can be induced after AdH1-K-ras^val12 infection. This kind of adenovirus based on RNAi might be a promising vector for cancer therapy. | Li-MoChen Huang-YingLe Ren-YiQin ManojKumar Zhi-YongDu Rui-JuanXia JingDeng | 2005 | World Journal of Gastroenterology2005，11，6： | 22 |
| 9 | 瞬时表达靶向TMV外壳蛋白基因的siRNA能干扰病毒侵染显示文摘RNA干扰(RNA interference,RNAi)是与内源性mRNA编码区某段序列同源的双链RNA导入细胞后,该mRNA发生特异性降解,从而导致该基因表达沉默的现象。小干扰RNA(small interfering RNA,siRNA)作为RNAi途径的重要中介, 已被广泛应用于动、植物抗病毒治疗研究。本文以烟草花叶病毒(Tobacco mosaic virus,TMV)外壳蛋白基因为靶位,设计合成表达小干扰RNA的寡核苷酸,亚克隆到植物双元表达载体pBI121中,直接转化根癌农杆菌。通过根癌农杆菌介导的瞬时表达法,研究了同源于TMV外壳蛋白的siRNA对TMV侵染的干扰作用。结果表明,瞬时表达的siRNA能够特异性干扰TMV侵染。含有重组表达载体pBI121/siRNA的根癌农杆菌渗入普通烟植株,在TMV接种后14 d其上部叶片没有表现典型的花叶症状。对这些叶片进行Northern杂交试验也没有检测到TMV病毒的RNA积累或仅有很少量的积累。在枯斑寄主心叶烟上,siRNA的瞬时表达可使TMV侵染后的枯斑数明显减少,甚至不产生枯斑。此外,同源于TMV外壳蛋白的siRNA瞬时表达对非同源的黄瓜花叶病毒(Cucumber mosaic virus,CMV)没有抑制作用,表明siRNA的干扰作用具有高度的同源依赖性。 | 赵明敏 安德荣 黄广华 何祖华 陈江野 | 2006 | 植物病理学报2006，36，1： | 22 |
| 10 | Inhibition of survivin expression and mechanisms of reversing drug-resistance of human lung adenocarcinoma cells by siRNA显示文摘背景 Survivin, apoptosis 的禁止者的一个成员蛋白质(国际机场) 家庭,在肿瘤房间并且不的 overexpresses 在严重地区分的成年纸巾表示。试图在 vitro 并且在 vivo 在房间增长, apoptosis 和 chemosensitivity 上调查 survivin 特定的 siRNA 的效果到 cisplatin 并且在颠倒癌症房间抵抗到化学疗法的 drug.Methods 关于 survivin 的减少的表示探索机制的这研究 Survivin 特定的 siRNA 是进 A549/DDP 房间的 transfected。抵抗相关的蛋白质( LRP ) mRNA 铺平的 survivin 和肺的表示被 RT-PCR 决定,到 cisplatin 的 A549/DDP ( cisplatin )房间的 chemosensitivity 被 MTT 试金决定,并且 apoptosis 和房间骑车被流动 cytometry ( FCM )决定 survivin 的 .The 蛋白质表示层次, LRP , cyclin-D1 , caspase-3 和 bcl-2 被西方的弄污的分析决定。肿瘤生长上的 survivin siRNA 抑制的效果在 vivo.Results 在 athymic 裸体人老鼠被学习 Survivin 特定的 siRNA 高效地下面调整的 survivin 表示。房间周期在 G2/M 阶段被逮捕,并且 apoptosis 显然被发现。survivin 表示的抑制能让 IC50 和 cisplatin 的药抵抗的索引减少,并且提高癌症房间敏感到 cisplatin。在由 survivin 特定的 siRNA 的 transfection 以后, LRP 和 cyclin-D1 的表示是 downregulated, caspase-3 表示是 upregulated,有的 bcl-2 表示没有明显的变化。survivin 击倒的证实的动物实验能禁止肿瘤 growth.Conclusions Survivin 特定的 siRNA 罐头高效地压制 survivin 的表示,增加 apoptosis,禁止细胞增长并且提高到在 vitro 并且在 vivo 的 cisplatin 的 chemosensitivity。survivin 表示帮助颠倒药抵抗的抑制可以与 LRP 的 downregulation 有关系, caspase-3.Anti-tumor 策略的 upregulation 可能在指向肺腺癌基于 survivin 的抑制是有用的。 | LIU Jing-lei WANG Yan JIANG Ji KONG Rui YANG Yan-mei JI Hong-fei SHI Yu-zhi | 2010 | Chinese Medical Journal2010，，20： | 22 |
| 11 | Metastasis-associated protein 1 induces VEGF-C and facilitates lymphangiogenesis in colorectal cancer显示文摘AIM:To study the correlation between high metastasisassociated protein 1(MTA1)expression and lymphangiogenesis in colorectal cancer(CRC)and its role in production of vascular endothelial growth factor-C(VEGF-C). METHODS:Impact of high MTA1 and VEGF-C expression levels on disease progression and lymphovasculardensity(LVD,D2-40-immunolabeled)in 81 cases of human CRC was evaluated by immunohistochemistry. VEGF-C mRNA and protein expressions in human LoVo and HCT116 cell lines were detected by real-time polymerase chain reaction and Western blotting,respectively,with a stable expression vector or siRNA. RESULTS:The elevated MTA1 and VEGF-C expression levels were correlated with lymph node metastasis and Dukes stages(P<0.05).Additionally,high MTA1 expression level was correlated with a large tumor size(P< 0.05).A significant correlation was found between MTA1 and VEGF-C protein expressions in tumor cells(r=0.371, P<0.05).Similar to the VEGF-C expression level,high MTA1 expression level was correlated with high LVD in CRC(P<0.05).Furthermore,over-expression of MTA1 significantly enhanced the VEGF-C mRNA and protein expression levels,whereas siRNAs-knocked down MTA1 decreased the VEGF-C expression level. CONCLUSION:MTA1,as a regulator of tumor-associated lymphangiogenesis,promotes lymphangiogenesis in CRC by mediating the VEGF-C expression. | Bin Du Zhen-Yu Yang Xue-Yun Zhon Mao Fang Yong-Rong Yan Guo-Long Qi Yun-Long Pan Xu-Long Zhou | 2011 | World Journal of Gastroenterology2011，17，9： | 23 |
| 12 | 高效siRNA设计的研究进展显示文摘RNA干扰(RNA interference,RNAi)是生物界普遍存在的一种抵御外来基因和病毒感染的保守进化机制,其本质是siRNA与靶向mRNA特异结合、并由RISC介导其降解,从而阻止mRNA的翻译,导致基因沉默。因此, RNAi可以作为基因功能研究、基因治疗等的新工具。但是,随机设计的siRNA之间沉默效应差别很大。如何针对靶基因设计特异、高效的siRNA就成了一个关键的问题。文章对siRNA设计原则的研究进展进行了总结论述。 | 许德晖 黄辰 刘利英 宋土生 | 2006 | 遗传2006，28，11： | 21 |
| 13 | RNA干扰技术的研究进展显示文摘RNA干扰是一项新的分子生物学技术,是外源和内源性双链RNA在生物体内诱导同源靶基因的mRNA特异性降解,从而导致转录后基因沉默的现象。尽管RNA干扰发现的时间较短,但由于其具有操作简单、成本低、特异性高和高效性等特点,因而发展迅速,目前对于它的机制已有初步的了解,同时RNA干扰在功能基因组学以及疾病的基因干预治疗方面也有一定的进展。该文就RNA干扰技术的历史、作用机制、生物学意义及应用作简要概述。 | 秦玉新 蒙凌华 丁健 | 2007 | 中国药理学通报2007，23，4： | 21 |
| 14 | Inhibition effect of small interfering RNA of connective tissue growth factor on the expression of vascular endothelial growth factor and connective tissue growth factor in cultured human peritoneal mesothelial cells显示文摘对腹分离的腹膜反应能导致的背景纤维变性。(TGF-1 ) 转变生长因素 1 在调整织物修理并且在损害以后改变起一个关键作用。结缔组织生长因素(CTGF ) ,导致纤维变性的 TGF-1 的一个下游的调停人,在腹纤维变性被含有。脉管的 endothelial 生长因素(VEGF ) 在能赶快的 angiogenesis 起一个关键作用腹纤维变性。在这研究,我们调查了 CTGF 的小介入 RNA ( siRNA )的效果由pRETRO超级( PRS )在人的腹的 CTGF 和 VEGF 的表示上的 retrovirus 向量生产 CTGF siRNA 的间皮的 cells.Methods Retrovirus 从转换 oligonucleotides 被构造并且转了进与 lipofectamine 包装房间线 PT67 ,并且病毒上层清液被用来感染人的腹间皮的房间( HPMC )。房间被划分成七个组:低葡萄糖 DMEM,低葡萄糖 DMEM + TGF-1 5 ng/ml,低葡萄糖 DMEM + TGF-1 5 ng/ml + PRS-CTGF-siRNA1-4 和低葡萄糖 DMEM + TGF-1 5 ng/ml + PRS。CTGF 和 VEGF 的表示被 semiquantitative RT-PCR 和 CTGF 的西方的 blot.Results 底层测量, VEGF 在汇合的 HPMC 被检测。有 TGF-1 的后面的刺激, CTGF 和 VEGF 的层次是显著地 upregulated (P0.01 ) 。PRS-CTGF-siRNA1-4 的介绍导致了 CTGF 的重要减小 mRNA 和蛋白质,和 VEGF mRNA (P0.01 ) ,特别在组 PRS-CTGF-siRNA1 和 PRS-CTGF-siRNA4。PRS 空向量的介绍没有这些效果(P0.05 ).Conclusions CTGF siRNA 的表示由 retrovirus 向量能有效地减少的 PRS 调停了 CTGF 和 VEGF 的水平在有教养的 HPMC 由 TGF-1 导致了。这研究可以提供潜在的治疗学的策略阻止腹纤维变性。 | LIU Fu-you XIAO Li PENG You-ming DUAN Shao-bin LIU Hong LIU Ying-hong LING Gui-hui YUAN Fang CHEN Jun-xiang FU Xiao ZHU Jian-lian | 2007 | Chinese Medical Journal2007，，3： | 20 |
| 15 | Identification of effective siRNA against K-ras in human pancreatic cancer cell line MiaPaCa-2 by siRNA expression cassette显示文摘AIM: We shall construct the small interfering RNA (siRNA)expression cassette (SEC) targeting activated K-ras gene sequence, identify more effective siRNA sequence against K-ras gene in human pancreatic cancer cell line MiaPaCa-2 by SEC and reveal the anti-cancer effects of RNA interference (RNAi) and its therapeutic possibilities.WETHODS: Three different sites of SECs were constructed by PCR. K1/siRNA, K2/siRNA and K3/siRNA are located at sites 194, 491 and 327, respectively. They were transfected into MiaPaCa-2 cells by liposome to inhibit the expression of activated K-ras. In the interfering groups of sites 194 and 491, we detected the apoptosis in cells by FACS after they were incubated for 48 h, then we tested the alternation of K-ras gene in MiaPaCa-2 cells by RT-PCR immunofluorescence, respectively.RESULTS: Introduction of the K1/siRNA and K2/siRNA against K-ras into MiaPaCa-2 cells leads to increased apoptosis, and the number of apoptotic cells is increased compared with control cells. The tests of RT-PCR immunofluorescence show the effects of inhibiting expression of activated K-ras gene by RNA interference in the K1/siRNA and K2/siRNA groups. We also find that the introduction of K3/siRNA has no effect on MiaPaCa-2 cells.CONCLUSION: K1/siRNA and K2/siRNA can inhibit the expression of activated K-fas but K3/siRNA has no effect,demonstrating that K1/siRNA and K2/siRNA are effective sequences against K-ras gene and K3/siRNA are not. We conclude that specific siRNA against K-ras expression may be a powerful tool to be used therapeutically against human pancreatic cancer. | WeiWang Chun-YouWang Ju-HuaDong XiongChen MinZhang GangZhao | 2005 | World Journal of Gastroenterology2005，11，13： | 20 |
| 16 | MicroRNA及其在人和动物上的研究进展显示文摘MicroRNA是一种长约22nt的非编码RNA,通过与靶基因的3′UTR区结合来调控靶基因的表达。目前已证实miRNA在生物体生长、发育和疾病发生等过程中发挥着重要的作用。文章介绍了miRNA的特征、作用机制,综述了关于miRNA的功能、miRNA基因的鉴定与靶基因预测的最新研究进展。 | 盛熙晖 杜立新 | 2007 | 遗传2007，29，6： | 20 |
| 17 | RNA干涉胰岛素样生长因子1类受体的研究显示文摘RNAi技术的关键是siRNA的制备,实验结果证实,通过发卡结构的小RNA(shRNA)载体表达siRNA可以抑制特定靶基因表达。我们通过将针对IGFIR基因的RNA干扰片段装入特定质粒PSUPER中,再转染入人肝癌细胞株SMMC7721中,并筛选出稳定株。 | 牛坚 钱海鑫 李向农 黄健 韩泽广 | 2006 | 中华实验外科杂志2006，23，7： | 19 |
| 18 | Inhibitory effects of miRNA-200c on chemotherapy-resistance and cell proliferation of gastric cancer SGC7901/DDP cells显示文摘Background and Objective: miRNA-200c can not only inhibit the aggressiveness of cancer cells but also increase the sensitivity of cells to antitumor drugs. However, some mechanisms are still unclear. Recent researches revealed that E-cadherin is more than an inhibitor of metastasis, and it also plays important roles in reversing drug resistance. We had previously found that miRNA-200c could not only induce the expression of E-cadherin but also increase the sensitivity of gastric cancer SGC7901/DDP cells to cisplatin (DDP). This study aimed to explore the effects of miRNA-200c on biological characteristics of SGC7901/DDP cells and the roles of E-cadherin in the regulatory pathway of miRNA-200c. Methods: SGC7901/DDP cells and its parental cell line SGC7901 cells were transfected with miRNA-200c precursor (Pre-200c) and E-cadherin siRNA, respectively. Real-time RT-PCR was used to detect miRNA-200c expression after transfection with Pre-200c in SGC7901/DDP cell line. Drug sensitivities to DDP, 5-fluorouracil (5-FU), paclitaxel, and adriamycin (ADR) after transfection were tested using MTT assay. The proliferation of SGC7901/DDP cells was also detected after transfection. The protein changes of E-cadherin, Bax, and Bcl-2 after transfection were detected by Western blot. Results: The miRNA-200c expression in SGC7901/DDP cells after transfection of Pre-200c was 7.128 ± 0.159 times of that in negative control (P < 0.05). The IC50 of DDP, 5-FU, paclitaxel, and ADR in Pre-200c-transfected group were significantly lower than that in negative control group (P < 0.05). Compared to the control group, cell proliferation was significantly decreased (P < 0.05). The relative protein expressions of E-cadherin and Bax in Pre-200c-transfected group were significantly higher than those in negative control group (P < 0.05), whereas Bcl-2 was significantly lower than that in control (P < 0.05). Additionally, E-cadherin protein expression was significantly inhibited after transfected with E-cadherin siRNA in SGC7901 cells. The Bax protein expression was significantly down-regulated by E-cadherin siRNA (P < 0.05), whereas the Bcl-2 expression was significantly up-regulated (P < 0.05). Conclusion: miRNA-200c can indirectly regulate apoptosis through E-cadherin in SGC7901/DDP cells, which may be a possible mechanism of miRNA-200c in reversing drug resistance and inhibiting proliferation. | Yong Chen Jing Zuo Ying Liu Hong Gao Wei Liu | 2010 | Chinese Journal of Cancer2010，29，12： | 18 |
| 19 | HMGB1及其受体RAGE分子信号通路参与调节肝细胞肝癌增殖和侵袭迁移机制的研究显示文摘目的观察高迁移率族蛋白B1(HMGB1)及其受体晚期糖基化终产物(RAGE)在人体肝细胞癌(HCC)组织中的表达情况,了解HMGB1及其受体RAGE对HCC细胞增殖和侵袭转移的影响,研究HMGB1及其受体分子信号通路参与调节HCC细胞增殖和侵袭转移的相关机制。方法选取10例人体HCC组织标本和HCC细胞培养标本,以正常的肝脏组织细胞作为对照。通过免疫荧光染色、Western blot、RT-PCR检查方法分析HMGB1对HCC细胞内丝裂原活化蛋白激酶(MAPKs)、蛋白激酶B(AKT)、NT-κB等信号通路的调节,检测HCC细胞中HMGB1及其受体分子RAGE蛋白的表达量,对HMGB1及其受体RAGE的表达量与其临床症状作相关性分析。结果 1在HMGB1抑制剂甘草皂甙、重组HMGB1(r HMGB1)、r HMGB1+sRAGE的作用下,能够有效干扰HMGB1在HCC细胞中的表达。干扰HMGB1可以抑制HCC细胞的增殖、促使细胞凋亡、引起细胞周期阻滞,同时降低其体外迀移和侵袭能力。这些结果提示HMGB1在HCC中具有促增殖、促迁移、抗凋亡和侵袭的作用。2HMGB1能增强MAPKs和NF-κB信号通路活性。稳定干扰HMGB1的HCCLM3细胞内MAPKs的磷酸化水平降低,包括p38和JNK,同时它们的上游激酶(MEK1/2、SEK1)和下游底物(c-Jun、-Myc)的磷酸化也被抑制;NF-κB的表达量及Ser536位点的磷酸化水平也下调。结论 1HMGB1与RAGE结合通过激活MAPK信号通路最终导致核转录因子NF-κB激活并促进RAGE基因转录,增加RAGE的mRNA含量,使RAGE表达上调,正反馈的扩大HMGB1引起的反应;2HMGB1通过作用于RAGE激活下游RAC1分子,并最终引起VEGF表达上调,进而促进HCC的增殖和侵袭转移。 | 刘清 丁光仁 惠永峰 严慧 王琦 | 2017 | 临床和实验医学杂志2017，16，3： | 17 |
| 20 | siRNA非病毒递送载体的研究现状显示文摘RNA干扰(RNA interference,RNAi)是近年发展起来的一种新技术。RNAi是指通过外源性或内源性的双链RNA在体内诱导靶基因mRNA产生特异性降解,进而引起不同水平的基因沉默。RNAi已经用于肿瘤、病毒感染、乙型肝炎等多种疾病的治疗。小干扰RNA(siRNA)是RNAi的效应分子,可在体内诱导RNAi效应。但是裸siRNA在体内容易被核酶(RNase)降解,且半衰期短,转染效率低。因此,siRNA需要借助递送载体进入细胞发挥治疗作用。病毒载体在基因治疗中有潜在的免疫原性、致突变等副作用。所以,非病毒载体成为当前的研究热点。本文对siRNA非病毒递送载体的研究现状进行了综述。 | 杨飞飞 黄伟 李云飞 高钟镐 | 2011 | 药学学报2011，46，12： | 17 |
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