A Method for Inducible Gene Over-Expression and Down-Regulation in Emerging Model Species Using Pogostick

2013 ◽  
pp. 249-266
Author(s):  
Bin Chen ◽  
Antónia Monteiro
Keyword(s):  
Model Species ◽  
Down Regulation ◽  
Over Expression ◽  
Inducible Gene

scholarly journals Pogostick: A New Versatile piggyBac Vector for Inducible Gene Over-Expression and Down-Regulation in Emerging Model Systems

PLoS ONE ◽  
2011 ◽  
Vol 6 (4) ◽  
pp. e18659 ◽  
Author(s):  
Bin Chen ◽  
Steven Hrycaj ◽  
Johannes B. Schinko ◽  
Ondrej Podlaha ◽  
Ernst A. Wimmer ◽  
...  
Keyword(s):  
Model Systems ◽  
Down Regulation ◽  
Over Expression ◽  
Piggybac Vector ◽  
Inducible Gene

scholarly journals Over-Expression of p45SKP2 in Kaposi’s Sarcoma Correlates with Higher Tumor Stage and Extracutaneous Involvement but Is Not Directly Related to p27KIP1 Down-Regulation

2002 ◽  
Vol 15 (11) ◽  
pp. 1227-1235 ◽  
Author(s):  
R. M. Penin ◽  
M. T. Fernandez-Figueras ◽  
L. Puig ◽  
J. Rex ◽  
C. Ferrandiz ◽  
...  
Keyword(s):  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Tumor Stage ◽  
Down Regulation ◽  
Over Expression

scholarly journals Over-expression of transcription factor ARK1 gene leads to down-regulation of lignin synthesis related genes in hybrid poplar ‘717’

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Qinxia Ye ◽  
Xiaozhen Liu ◽  
Wen Bian ◽  
Zhiming Zhang ◽  
Hanyao Zhang
Keyword(s):  
Transcription Factor ◽  
Hybrid Poplar ◽  
Down Regulation ◽  
Over Expression ◽  
Lignin Synthesis

scholarly journals MicroRNAs in mouse models of lymphoid malignancies

2010 ◽  
Vol 1 (1) ◽  
pp. 8 ◽  
Author(s):  
Nicola A. O. Zanesi ◽  
Yuri Pekarsky ◽  
Francesco Trapasso ◽  
George Calin ◽  
Carlo M. Croce
Keyword(s):  
Gene Expression ◽  
Mouse Models ◽  
Gene Expression Regulation ◽  
Human Leukemia ◽  
Down Regulation ◽  
Over Expression ◽  
Lymphoid Malignancies ◽  
Knockout Animals ◽  
Mouse Modeling

<!--StartFragment--> <p class="MsoBodyText"><span style="mso-tab-count: 1;"> </span>The discovery of microRNAs (miRNAs) has revealed a new layer of gene expression regulation that affects many normal and pathologic biological systems. Among the malignancies affected by the dysregulation of miRNAs there are cancers of lymphoid origin, in which miRNAs are thought to have tumor suppressive or tumor promoting activities, depending on the nature of their specific targets. In the last 4-5 years, the experimental field that provided the deepest insights into the <em>in vivo</em><span style="font-style: normal;"> biology of miRNAs is that of mouse modeling in which transgenic and knockout animals mimic, respectively, over-expression or down-regulation of specific miRNAs involved in human leukemia/lymphoma. This review discusses recent advances in our understanding of lymphoid malignancies based on the natural and engineered mouse models of three different miRNAs, miR-15a/16-1 cluster, miR-155, and miR-17-92 cluster.</span></p> <!--EndFragment-->

scholarly journals MicroRNA-101 inhibits growth and metastasis of human ovarian cancer cells by targeting PI3K/AKT

2021 ◽  
Vol 17 (1) ◽  
pp. 127-134
Author(s):  
Min Wei ◽  
Hongjuan Jin ◽  
ShuLi Yang ◽  
Zhuo Li ◽  
Xinlei Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cancer Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Pten Expression ◽  
Cell Cycle Analysis ◽  
Ovarian Cancer Cells ◽  
G1 Arrest ◽  
Down Regulation ◽  
Over Expression

IntroductionOvarian cancer is the most frequent cause of gynecological cancer related mortality in woman. This study was designed to investigate the role and therapeutic potential of miRNA-101 in ovarian cancer.Material and methodsExpression analysis was carried out by real-time quantitative polymerase chain reaction. Transfections were performed with the help of Lipofectamine 2000 reagent. AO/EB and annexin V/PI staining was used to detect apoptosis and flow cytometry was used for cell cycle analysis. Western blotting was employed for cell cycle analysis.ResultsIt was found that miRNA-101 was significantly down-regulated in ovarian cancer cells. The over-expression of miRNA-101 causes a significant decrease in the viability of ovarian cancer cells via the initiation of apoptosis and sub-G1 arrest of OVACAR-3 cells. It was indicated that PTEN was the potential target of miRNA-101 in OVACAR-3 cells. There was 4.5-fold up-regulation of PTEN expression in ovarian cancer cell lines and the over-expression of miRNA-101 in OVACAR-3 cells resulted in the down-regulation of PTEN expression. The inhibition of PTEN in the OVACAR-3 cells arrested the proliferation of these cells. The over-expression of miRNA-101 causes significant down-regulation in PI3K and AKT expression of OVACAR-3 cells.ConclusionsIt can be concluded that miRNA-101 acts as a tumor suppressor which may be beneficial in the treatment of ovarian cancer.

Valproic acid (VPA) enhances cisplatin sensitivity of non-small cell lung cancer cells via HDAC2 mediated down regulation of ABCA1

2017 ◽  
Vol 398 (7) ◽  
pp. 785-792 ◽  
Author(s):  
Jian-Hui Chen ◽  
Yu-Long Zheng ◽  
Chuan-Qin Xu ◽  
Li-Zhi Gu ◽  
Zong-Li Ding ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Valproic Acid ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Luciferase Reporter ◽  
Small Cell Lung ◽  
Down Regulation ◽  
Over Expression ◽  
Protein Levels

Abstract Valproic acid (VPA) has been suggested to be a histone deacetylase inhibitor (HDACI). Our present study revealed that VPA at 1 mm, which had no effect on cell proliferation, can significantly increase the sensitivity of non-small cell lung cancer (NSCLC) cells to cisplatin (DDP). VPA treatment markedly decreased the mRNA and protein levels of ABCA1, while had no significant effect on ABCA3, ABCA7 or ABCB10. Luciferase reporter assays showed that VPA can decrease the ABCA1 promoter activity in both A549 and H358 cells. VPA treatment also decreased the phosphorylation of SP1, which can bind to −100 and −166 bp in the promoter of ABCA1. While the phosphorylation of c-Fos and c-Jun were not changed in VPA treated NSCLC cells. Over expression of HDAC2 attenuated VPA induced down regulation of ABCA1 mRNA expression and promoter activities. Over expression of HDAC2 also attenuated VPA induced DDP sensitivity of NSCLC cells. These data revealed that VPA can increase the DDP sensitivity of NSCLC cells via down regulation of ABCA1 through HDAC2/SP1 signals. It suggested that combination of VPA and anticancer drugs such as DDP might be great helpful for treatment of NSCLC patients.

The Down-Regulation of Neuroligin-2 and the Correlative Clinical Significance of Serum GABA Over-Expression in Hirschsprung’s Disease

2014 ◽  
Vol 39 (8) ◽  
pp. 1451-1457 ◽  
Author(s):  
Hongchao Yang ◽  
Jianyi Niu ◽  
Jian Wang ◽  
Fan Zhang ◽  
Qiangye Zhang ◽  
...  
Keyword(s):  
Clinical Significance ◽  
Hirschsprung's Disease ◽  
Hirschsprung’S Disease ◽  
Down Regulation ◽  
Over Expression

scholarly journals The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

2017 ◽  
Vol 41 (6) ◽  
pp. 2489-2502 ◽  
Author(s):  
Bo Yu ◽  
Xuan Ye ◽  
Qiong Du ◽  
Bin Zhu ◽  
Qing Zhai
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Over Expression ◽  
Non Coding Rna ◽  
Colorectal Cancer Cells ◽  
Long Non Coding Rna

Background/Aims: The long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) contributes to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer remains unknown. In the present study, we investigated whether CRNDE was involved in the development of colorectal cancer via the binding of microRNA (miR)-217 with transcription factor 7-like 2 (TCF7L2) to enhance the Wnt signaling pathway. Methods: Quantitative polymerase chain reaction was used to detect CRNDE, miR-217 and TCF7L2 in colorectal cancer tissues and cells. The CCK-8 assay, wound healing assay, and Transwell assay were used to detect cell proliferation, migration and invasion, respectively. Western blotting and luciferase activity assays were used to identify CRNDE and TCF7L2 as one of the direct targets of miR-217. The activity of the Wnt/β-catenin signaling pathway was analyzed by the TOPflash assay, and the subcellular localization of β-catenin and TCF7L2 was analyzed by western blotting and confocal microscopy. Results: In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. CRNDE down-regulation inhibited the cell proliferation, migration and invasion in vitro and in vivo and the inhibitions were both completely blocked after miR-217 inhibition or TCF7L2 overexpression. Finally, TOPflash analysis showed that the activity of Wnt/β-catenin signaling is inhibited by CRNDE down-regulation and rescued by TCF7L2 over-expression. Consistently immunostaining and western blotting analysis showed that the expression of b-catenin and TCF7L2 in the nucleus was significantly decreased by CRNDE down-regulation and was rescued by TCF7L2 over-expression. Conclusions: The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/β-catenin signaling through binding miR-217 competitively.

Over-expression of Reticulon 3 (RTN3) enhances TRAIL-mediated apoptosis via up-regulation of death receptor 5 (DR5) and down-regulation of c-FLIP

2009 ◽  
Vol 279 (2) ◽  
pp. 185-192 ◽  
Author(s):  
Jung Tae Lee ◽  
Tae-Jin Lee ◽  
Cheol-Hee Kim ◽  
Nam-Soon Kim ◽  
Taeg Kyu Kwon
Keyword(s):  
Death Receptor ◽  
Death Receptor 5 ◽  
Down Regulation ◽  
Over Expression
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