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| 1 | Grhl3 induces human epithelial tumor cell migration and invasion via downregulation of E-cadherin显示文摘Grainyhead 基因涉及愈合弯屈和发展神经试管闭合。转移在细胞从主要肿瘤的地点传播哪个癌症并且在远器官建立第二等的肿瘤期间是一个 multistep 过程。粘附蛋白质 E-cadherin 在转移起一个必要作用。考虑到在在皮或乳癌发生在侵略的获得期间的愈合创伤的过程和 EMT 发生的 epithelialmesenchymal 转变(EMT ) 的类似的高度,我们在癌症侵略调查了 Grainyhead 基因的角色。这里,我们证明在象 Grainyhead 一样之间有一种反的关系 3 (Grhl3 ) 并且在某上皮的肿瘤房间的 E-cadherin 表示排队。在 E-cadherin-positive 上皮的肿瘤房间线的 Grhl3 的 Overexpression,由更少的侵略描绘了,产生了 E-cadherin 基因的 transcriptional 阻塞并且支持了房间移植和房间侵略。相反地, Grhl3 弄空禁止了房间移植和房间侵略并且与 E-cadherin 表示的获得被联系。为了推进,探索 Grhl3 由调整了 E-cadherin 表示的机制, E-cadherin 倡导者报告分析被表现,结果出现了那 Grhl3 镇压 E-cadherin 基因表示由对在近似 E-cadherin 倡导者在场的电子盒子直接或间接地有约束力。一起拿,我们的调查结果在癌症房间由 E-cadherin 的 downregulation 在移植和侵略的正式就职为 Grhl3 定义一个主要角色。 | Pan Zhao Sijia Guo Zhenzhen Tu Lijun Di Xiaoiun Zha Haisheng Zhou Xuejun Zhang | 2016 | Acta Biochimica et Biophysica Sinica2016，0，3： | 9 |
| 2 | Impaired tumor angiogenesis and VEGF- induced pathway in endothelial CD146 knockout mice显示文摘 | Qiqun Zeng Zhenzhen Wu Hongxia Duan Xuan Jiang Tao Tu Di Lu Yongting Luo Ping Wang Lina Song Jing Feng Dongling Yang Xiyun Yan | 2014 | Protein & Cell2014，5，6： | 6 |
| 3 | AEG1通过激活NF-κB和AP-1诱导肝癌HepG2细胞COX-2表达(英文)显示文摘Objective:The aim of this study was to investigate whether astrocyte elevated gene 1 (AEG1) regulates COX-2 expression in human hepatoma HepG2 cells and related pathways involved in this process. Methods:Human hepatoma HepG2 cells were transfected with pcDNA3.1(-)-AEG1 plasmid or psilencer2.0-AEG1-shRNA1 plasmid to up/down-regulate AEG1 expression, pcDNA3.1(-) and psilencer 2.0 empty vector plasmids were transfected respectively as control. Real-time RT-PCR was carried out to measure the expression levels of AEG1 and COX-2 mRNA. The expression levels of AEG1 and COX-2 protein were detected by Western blot. NF-κB signaling was blocked by PDTC, and AP-1 signaling was blocked by curcumin. Results:AEG1 mRNA and protein levels were increased after pcDNA3.1(-)-AEG1 transfection, and decreased after psilencer2.0-AEG1-shRNAs transfection. COX-2 mRNA and protein levels were increased in AEG1-overexpressing cells and decreased in AEG1-knockdown cells. Phosphorylations of p65 and c-jun were up-regulated in AEG1-overexpressing cells. Both PDTC and curcumin reduced COX-2 expression in HepG2 cells with AEG1 overexpression. Conclusion:AEG1-overexpressing and-knockdown HepG2 cells are established successfully. AEG1 could induce COX-2 expression though activating NF-κB and AP-1 in human hepatoma HepG2 cells. | Huan Deng Zhenzhen Zhou Wei Tu Yujia Xia Huanjun Huang De'an Tian | 2013 | The Chinese-German Journal of Clinical Oncology2013，12，6： | 2 |
| 4 | A bioinformatics method for predicting long noncoding RNAs associated with vascular disease显示文摘Long noncoding RNAs(lncRNAs)play important roles in human diseases including vascular disease.Given the large number of lncRNAs,however,whether the majority of them are associated with vascular disease remains unknown.For this purpose,here we present a genomic location based bioinformatics method to predict the lncRNAs associated with vascular disease.We applied the presented method to globally screen the human lncRNAs potentially involved in vascular disease.As a result,we predicted 3043 putative vascular disease associated lncRNAs.To test the accuracy of the method,we selected 10 lncRNAs predicted to be implicated in proliferation and migration of vascular smooth muscle cells(VSMCs)for further experimental validation.The results confirmed that eight of the 10 lncRNAs(80%)are validated.This result suggests that the presented method has a reliable prediction performance.Finally,the presented bioinformatics method and the predicted vascular disease associated lncRNAs together may provide helps for not only better understanding of the roles of lncRNAs in vascular disease but also the identification of novel molecules for the diagnosis and therapy of vascular disease. | LI JianWei GAO Cheng WANG YuChen MA Wei TU Jian WANG JunPei CHEN ZhenZhen KONG Wei CUI QingHua | 2014 | Science China(Life Sciences)2014，57，8： | 2 |
| 5 | Therapeutic effect of the treatment for colorectal cancer with adenoviral vectors mediated estrogen receptor β gene therapy combined with thermotherapy显示文摘 | Zhenzhen Tu Yuxiang Ma Walter Akers Samuel Achilefu Yueqing Gu | 2014 | Journal of Cancer Research and Clinical Oncology2014，，4： | 1 |
| 6 | Netrin-1 Induces Epithelial–Mesenchymal Transition and Promotes Hepatocellular Carcinoma Invasiveness显示文摘 | Wei Yan Ping Han Zhenzhen Zhou Wei Tu Jiazhi Liao Peiyuan Li Mei Liu Dean Tian Yu Fu | 2014 | Digestive Diseases and Sciences2014，，6： | 1 |
| 7 | Use of recombinant microRNAs as antimetabolites to inhibit human non-small cell lung cancer显示文摘During the development of therapeutic microRNAs(miRNAs or miRs),it is essential to define their pharmacological actions.Rather,miRNA research and therapy mainly use miRNA mimics synthesized in vitro.After experimental screening of unique recombinant miRNAs produced in vivo,three lead antiproliferative miRNAs against human NSCLC cells,miR-22-3p,miR-9-5p,and miR-218-5p,were revealed to target folate metabolism by bioinformatic analyses.Recombinant miR-22-3p,miR-9-5p,and miR-218-5p were shown to regulate key folate metabolic enzymes to inhibit folate metabolism and subsequently alter amino acid metabolome in NSCLC A549 and H1975 cells.Isotope tracing studies further confirmed the disruption of one-carbon transfer from serine to folate metabolites by all three miRNAs,inhibition of glucose uptake by miR-22-3p,and reduction of serine biosynthesis from glucose by miR-9-5p and-218-5p in NSCLC cells.With greater activities to interrupt NSCLC cell respiration,glycolysis,and colony formation than miR-9-5p and-218-5p,recombinant miR-22-3p was effective to reduce tumor growth in two NSCLC patient-derived xenograft mouse models without causing any toxicity.These results establish a common antifolate mechanism and differential actions on glucose uptake and metabolism for three lead anticancer miRNAs as well as antitumor efficacy for miR-22-3p nanomedicine,which shall provide insight into developing antimetabolite RNA therapies. | Yixin Chen Mei-Juan Tu Fangwei Han Zhenzhen Liu Neelu Batra Primo N.Lara Hong-Wu Chen Huichang Bi Ai-Ming Yu | 2023 | Acta Pharmaceutica Sinica B2023，13，10： | 0 |
| 8 | Nanoengineered Gallium Ion Incorporated Formulation for Safe and Efficient Reversal of PARP Inhibition and Platinum Resistance in Ovarian Cancer显示文摘Platinum-based chemotherapy remains the main systemic treatment of ovarian cancer(OC).However,the inevitable development of platinum and poly(adenosine diphosphate-ribose)polymerase inhibitor(PARPi)resistance is associated with poor outcomes,which becomes a major obstacle in the management of this disease.The present study developed“all-in-one”nanoparticles that contained the PARPi olaparib and gallium(Ga)(III)(olaparib-Ga)to effectively reverse PARPi resistance in platinum-resistant A2780-cis and SKOV3-cis OC cells and in SKOV3-cis tumor models.Notably,the olaparib-Ga suppressed SKOV3-cis tumor growth with negligible toxicity.Moreover,the suppression effect was more evident when combining olaparib-Ga with cisplatin or carboplatin,as evaluated in A2780-cis and SKOV3-cis cells.Mechanistically,the combined treatment induced DNA damage,which elicited the activation of ataxia telangiectasia mutated(ATM)/AMT-and Rad3-related(ATR)checkpoint kinase 1(Chk1)/Chk2 signal transduction pathways.This led to the arrest of cell cycle progression at S and G2/M phases,which eventually resulted in apoptosis and cell death due to unrepairable DNA damage.In addition,effective therapeutic responses to olaparib-Ga and cisplatin combination or olaparib-Ga and carboplatin combination were observed in SKOV3-cis tumor-bearing animal models.Altogether,the present findings demonstrate that olaparib-Ga has therapeutic implications in platinum-resistant OC cells,and the combination of olaparib-Ga with cisplatin or carboplatin may be promising for treating patients with OC who exhibit resistance to both PARPi and platinum. | Yangyang Li Yixuan Cen Mengyan Tu Zhenzhen Xiang Sangsang Tang Weiguo Lu Hongbo Zhang Junfen Xu | 2023 | Research2023，，3： | 0 |
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