The inhibitory effect of rBCG on EB virus-positive tumours using an EB virus fusion gene

2021 ◽  
Author(s):  
Qing-jie Xue ◽  
Hong-xia Yu ◽  
Ang Liu ◽  
Hui Wang ◽  
Yun-qing Li ◽  
...  
Keyword(s):  
Fusion Gene ◽  
Inhibitory Effect ◽  
Eb Virus ◽  
Virus Fusion

scholarly journals Molecular Evolution of Respiratory Syncytial Virus Fusion Gene, Canada, 2006–2010

2012 ◽  
Vol 18 (1) ◽  
pp. 120-124 ◽  
Author(s):  
Jesse Papenburg ◽  
Julie Carbonneau ◽  
Marie-Ève Hamelin ◽  
Sandra Isabel ◽  
Xavier Bouhy ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Molecular Evolution ◽  
Fusion Gene ◽  
Virus Fusion ◽  
Syncytial Virus

scholarly journals Translational enhancing activity in 5′ UTR of peste des petits ruminants virus fusion gene

FEBS Journal ◽  
2013 ◽  
Vol 280 (5) ◽  
pp. 1237-1248 ◽  
Author(s):  
Songkhla Chulakasian ◽  
Tien-Jye Chang ◽  
Ching-Hsiu Tsai ◽  
Min-Liang Wong ◽  
Wei-Li Hsu
Keyword(s):  
Fusion Gene ◽  
Peste Des Petits Ruminants ◽  
Virus Fusion

scholarly journals Liposomal delivery of methylphosphonate antisense oligodeoxynucleotides in chronic myelogenous leukemia [see comments]

Blood ◽  
1994 ◽  
Vol 84 (2) ◽  
pp. 601-607 ◽  
Author(s):  
AM Tari ◽  
SD Tucker ◽  
A Deisseroth ◽  
G Lopez-Berestein
Keyword(s):  
Growth Inhibition ◽  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Fusion Gene ◽  
Hematologic Malignancy ◽  
Control Cell ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
Myelogenous Leukemia ◽  
Ph Chromosome

Abstract Chronic myelogenous leukemia (CML) is a hematologic malignancy characterized by the presence of the Philadelphia (Ph) chromosome. Bcr- abl, the fusion gene associated with the Ph chromosome, expresses a p210bcr-abl protein that promotes a selective expansion of mature myeloid progenitor cells. Methylphosphonate (MP) oligodeoxynucleotides complementary to specific regions of the bcr-abl mRNA were incorporated in liposomes. We studied the effects of liposomal MP (L-MP) on the growth inhibition of CML-like cell lines. L-MP targeted to the breakpoint junctions of the bcr-abl mRNA inhibited the growth of CML cells. Fifty percent inhibition was achieved at approximately 1 mumol/L of L-MP oligonucleotide concentrations. The inhibitory effect was selective because growth inhibition was observed only with CML but not with control cell lines. Moreover, CML cell growth inhibition was dependent on the sequence of the MP oligodeoxynucleotides incorporated in the liposomes. The growth inhibition of CML cells by L-MP resulted from selective inhibition of the expression of the p210bcr-abl protein.

scholarly journals Alterations in Mitochondrial and Inflammasome Homeostasis by 2-Chloroethyl Ethyl Sulfide and their Mitigation by Curcumin: An In vitro Study

2021 ◽  
Author(s):  
Azam Kia ◽  
Mona Nadi ◽  
Vahideh Hajhasan ◽  
Jafar Salimian
Keyword(s):  
Sulfur Mustard ◽  
Fusion Gene ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
In Vitro Study ◽  
Inhibitory Effect ◽  
Epithelial Cell Line ◽  
Complete Suppression ◽  
Mitofusin 2

The mitochondrion has a substantial role in innate immunity and inflammasome signaling pathways. Sulfur mustard (SM) induces toxicity in cytoplasmic organelles. We aimed to evaluate the potential therapeutic effect of curcumin on the toxicity of SM analog through measuring gene expression levels of mitochondrial dynamics followed by induction of the inflammasome signaling pathway. After the treatment of pulmonary epithelial cell line (A549) by 2-chloroethyl ethyl sulfide (CEES) (2500 mM) for 48h, the transcriptional activity of mitochondrial fission and fusion genes such as dynamin-related protein 1 (Drp1), mitochondrial fission 1 protein (Fis1), mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and Dominant optic atrophy (Opa1) and inflammasome pathway genes including absent in melanoma 2 (AIM2), NLR family containing protein 3 (NLRP3), and Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) was measured. Furthermore, the inhibitory effect of curcumin (160 mM) concurrent with SM analog on the expression level of mitochondria and inflammasome genes was investigated. CEES was able to over-express the fission, fusion (Drp1 ~ 8, Fis1 4.5, Mfn2 15, and Opa1 16-fold) and inflammasome genes (AIM2, NLRP3, 8 and 6-fold, respectively), whereas Mfn1 was significantly decreased (0.5-fold) and a not statistically significant decrease was observed in the ASC gene. Curcumin could modulate the effect of CEES, mitigate the expression of fission, fusion, and inflammasome genes exceedingly. However, a major increase in the repairer fusion gene (Mfn1, 6-fold) and complete suppression of the ASC gene were the outcomes of using the curcumin. In conclusion, we suggest curcumin alleviates the disturbance of mitochondrial dynamics and downregulates the inflammasome genes exposed to the CEES.  

scholarly journals Targeted Inhibitory Effect of Nasopharyngeal Carcinoma Cells by Hre2.Grp78 Chimeric Promoter Regulating Fusion Gene TK/VP3

2019 ◽  
Vol 18 ◽  
pp. 153303381987516
Author(s):  
Jin-Yun Li ◽  
Wen-Xiao Huang ◽  
Jie Chen ◽  
Su-Ping Zhao ◽  
Yao-Yun Tang
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Fusion Gene ◽  
Quantitative Polymerase Chain Reaction ◽  
Hypoxia Inducible Factor ◽  
Glucose Deprivation ◽  
Inhibitory Effect ◽  
Carcinoma Cells ◽  
Chimeric Promoter ◽  
Hypoxia Inducible Factor 1Α ◽  
In Cells

Objective: To construct plasmids with Hre2.Grp78 chimeric promoter regulating fusion gene TK/VP3 and elaborate the effects of overexpressed TK/VP3 on nasopharyngeal carcinoma cells. Methods: Four plasmids were constructed, including pcDNA3.1-CMV-TK/VP3, pcDNA3.1-Hre2.TK/VP3, pcDNA3.1-Grp78.TK/VP3, and pcDNA3.1-Hre2.Grp78.TK/VP3. The human nasopharyngeal carcinoma cell line HNE1 cells were transfected with the 4 plasmids, respectively. Cell viabilities were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and apoptosis was conducted using flow cytometry analysis. The expression of TK, VP3, Grp78, and hypoxia-inducible factor 1α and apoptosis-related proteins was determined by real-time quantitative polymerase chain reaction and Western blotting. Results: The recombinant plasmids that could steadily overexpress TK and VP3 were successfully constructed. Expression of TK and VP3 in cells transfected with pcDNA3.1-Hre2.TK/VP3 and pcDNA3.1-Grp78.TK/VP3 was significantly higher than pcDNA3.1-CMV-TK/VP3, and expression in cells transfected with pcDNA3.1-Hre2.Grp78.TK/VP3 was the highest. Under glucose deprivation or hypoxia condition, Grp78 or hypoxia-inducible factor 1α was overexpressed so that expression of TK and VP3 was significantly upregulated, which could further inhibit cell proliferation and enhance cell apoptosis. Conclusion: We successfully constructed 4 plasmids with Hre2.Grp78 chimeric promoter regulating fusion gene TK/VP3, which could significantly inhibit the proliferation as well as enhance the apoptosis of nasopharyngeal carcinoma cells under glucose deprivation or hypoxia condition.

scholarly journals Hepatocyte nuclear factor-1 acts as an accessory factor to enhance the inhibitory action of insulin on mouse glucose-6-phosphatase gene transcription

1998 ◽  
Vol 95 (16) ◽  
pp. 9208-9213 ◽  
Author(s):  
Ryan S. Streeper ◽  
Erin M. Eaton ◽  
Daniel H. Ebert ◽  
Stacey C. Chapman ◽  
Christina A. Svitek ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Fusion Gene ◽  
Insulin Response ◽  
Inhibitory Effect ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Promoter Regions ◽  
Gene Encoding ◽  
Accessory Factor ◽  
Nuclear Factor 1

Glucose-6-phosphatase catalyzes the terminal step in the gluconeogenic and glycogenolytic pathways. Transcription of the gene encoding the glucose-6-phosphatase catalytic subunit (G6Pase) is stimulated by cAMP and glucocorticoids whereas insulin strongly inhibits both this induction and basal G6Pase gene transcription. Previously, we have demonstrated that the maximum repression of basal G6Pase gene transcription by insulin requires two distinct promoter regions, designated A (from −271 to −199) and B (from −198 to −159). Region B contains an insulin response sequence because it can confer an inhibitory effect of insulin on the expression of a heterologous fusion gene. By contrast, region A fails to mediate an insulin response in a heterologous context, and the mutation of region B within an otherwise intact promoter almost completely abolishes the effect of insulin on basal G6Pase gene transcription. Therefore, region A is acting as an accessory element to enhance the effect of insulin, mediated through region B, on G6Pase gene transcription. Such an arrangement is a common feature of cAMP and glucocorticoid-regulated genes but has not been previously described for insulin. A combination of fusion gene and protein-binding analyses revealed that the accessory factor binding region A is hepatocyte nuclear factor-1. Thus, despite the usually antagonistic effects of cAMP/glucocorticoids and insulin, all three agents are able to use the same factor to enhance their action on gene transcription. The potential role of G6Pase overexpression in the pathophysiology of MODY3 and 5, rare forms of diabetes caused by hepatocyte nuclear factor-1 mutations, is discussed.

scholarly journals Liposomal delivery of methylphosphonate antisense oligodeoxynucleotides in chronic myelogenous leukemia [see comments]

Blood ◽  
1994 ◽  
Vol 84 (2) ◽  
pp. 601-607 ◽  
Author(s):  
AM Tari ◽  
SD Tucker ◽  
A Deisseroth ◽  
G Lopez-Berestein
Keyword(s):  
Growth Inhibition ◽  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Fusion Gene ◽  
Hematologic Malignancy ◽  
Control Cell ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
Myelogenous Leukemia ◽  
Ph Chromosome

Chronic myelogenous leukemia (CML) is a hematologic malignancy characterized by the presence of the Philadelphia (Ph) chromosome. Bcr- abl, the fusion gene associated with the Ph chromosome, expresses a p210bcr-abl protein that promotes a selective expansion of mature myeloid progenitor cells. Methylphosphonate (MP) oligodeoxynucleotides complementary to specific regions of the bcr-abl mRNA were incorporated in liposomes. We studied the effects of liposomal MP (L-MP) on the growth inhibition of CML-like cell lines. L-MP targeted to the breakpoint junctions of the bcr-abl mRNA inhibited the growth of CML cells. Fifty percent inhibition was achieved at approximately 1 mumol/L of L-MP oligonucleotide concentrations. The inhibitory effect was selective because growth inhibition was observed only with CML but not with control cell lines. Moreover, CML cell growth inhibition was dependent on the sequence of the MP oligodeoxynucleotides incorporated in the liposomes. The growth inhibition of CML cells by L-MP resulted from selective inhibition of the expression of the p210bcr-abl protein.

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