1,554 research outputs found
Frequently rearranged in advanced T-cell lymphomas-1 demonstrates oncogenic properties in prostate cancer
No full textDownregulation of survivin by RNAi inhibits the growth of esophageal carcinoma cells.
No full textEsophageal squamous cell carcinoma ranks among one of the most frequent cause of cancer death in the world. Understanding of the molecular mechanisms involved in the pathogenesis of esophageal cancer becomes critical to develop more effective treatments. Elevated expression of survivin in esophageal carcinoma has been reported before and suppression of survivin expression leads to many tumor cells growth inhibition. We hypothesized that downregulation of survivin would inhibit the growth of human esophageal cancer cells. RNA interference directed against survivin was introduced into a human esophageal squamous cell carcinoma cell line KYSE510. Stable clones were selected and western blot analysis was performed to detect the protein level of survivin. Tumor cell growth in vitro and in vivo was assessed by trypan blue exclusion and nude mice experiments. Annexin V/propidium iodide staining followed by flow cytometric analysis and TUNEL assay were used to detect apoptosis in cell culture and in nude mice. We found that RNA interference could efficiently and stably suppress survivin expression in KYSE510 cells. Downregulation of survivin resulted in significantly inhibition of tumor growth in vitro and in vivo. The mechanism appears to be increased induction of apoptosis. Our results suggest a potential role for the targeting of survivin in the treatments of esophageal carcinoma
Development and optimisation of a duplex real-time reverse transcription quantitative PCR assay targeting the VP7 and NS2 genes of African horse sickness virus
No full textNucleotide sequences of 52 South African isolates of African horse sickness virus (AHSV) collected during 2004–2005 and including viruses of all nine AHSV serotypes, were used to design and develop a duplex real-time reverse transcription quantitative PCR (RT-PCR) assay targeting the VP7 (S8) and NS2 (S9) genes of AHSV. The assay was optimized for detection of AHSV in fresh and frozen blood of naturally infected horses. Assay performance was enhanced using random hexamers rather than gene-specific primers for RT, and with denaturation of double-stranded RNA in the presence of random hexamers. The assay was efficient with a linear range of at least five orders of magnitude. The analytical sensitivity of the assay was 132 copies of the target genes (4125 copies per ml of blood), and the assay was at least 10-fold more sensitive than virus isolation on BHK-21 cells. The assay was also highly specific because it did not detect related orbiviruses, such as bluetongue and equine encephalosis viruses.ID: S0166093410000893; M3: Article; Accession Number: S0166093410000893; Author: M. Quan (a, b, ⁎); Author: C.W. Lourens (a, b); Author: N.J. MacLachlan (c); Author: I.A. Gardner (d); Author: A.J. Guthrie (a); Affiliation: Equine Research Centre, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort 0110, South Africa; Affiliation: Department of Veterinary Tropical Diseases, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort 0110, South Africa; Affiliation: Equine Viral Disease Laboratory, Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA; Affiliation: Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA; Keyword: African horse sickness virus; Keyword: Real-time quantitative RT-PCR; Keyword: VP7 gene; Keyword: NS2 gene; Keyword: Duplex; Number of Pages: 8; Language: English
EB1 acts as an oncogene via activating ?-catenin/TCF pathway to promote cellular growth and inhibit apoptosis
No full textPreviously we showed that end-binding protein 1 (EB1) may promote cellular growth by activating ?-catenin/T-cell factor (TCF) pathway. To further investigate the role of EB1 in regulating cellular growth, we established an EB1-inducible expression system in which the protein level of EB1 was significantly upregulated upon doxycycline induction. We found that EB1 promoted cellular growth and resulted in a significant increase in colony formation. In addition, EB1 could induce tumor formation in nude mice, activate ?-catenin-dependent gene expression and upregulate the transcriptional activity of c-myc. We also showed that EB1 in this manner inhibited apoptosis of 293-T-REx cells upon cisplatin and upregulated expression of Bcl-2, whereas ?N TCF4, an inhibitor of ?-catenin/TCF pathway, could completely or partially abolish the effects of EB1 on the promotion of cell growth and the inhibition of apoptosis activity. Moreover, knockdown of c-myc by RNAi could abrogate upregulation of EB1-dependent induction of Bcl-2 expression. Overall, EB1 acts as a potential oncogene via activating ?-catenin/TCF pathway to promote cellular growth and inhibit apoptosis
Accumulation of cytoplasmic beta-catenin correlates with reduced expression of E-cadherin, but not with phosphorylated Akt in esophageal squamous cell carcinoma: immunohistochemical study
No full textAccumulation of β-catenin in cytoplasm occurs frequently during the pathogenesis of esophageal squamous cell carcinoma (ESCC). The mechanism leading to this alteration, however, is largely unknown. In the present study, immunohistochemistry was performed for β-catenin, E-cadherin and Ser473 phosphorylated Akt (P-Akt) in 44 tissue samples of ESCC and corresponding normal esophageal epithelium. Exon 3 of the β-catenin gene was analyzed by using single-strand conformation polymorphism and direct sequencing. In addition to the reduced expression of E-cadherin and membranous β-catenin observed in 65.9% and 68% of ESCC tested, respectively, cytoplasmic accumulation of β-catenin was also detected in 68% (30/44) cases. However, only two cases were found to have the same β-catenin gene mutation. The data showed that cytoplasmic accumulation of β-catenin was significantly associated with reduced expression of E-cadherin (P < 0.05) and that of membranous β-catenin (P < 0.05). Furthermore, cytoplasmic β-catenin was correlated significantly with lymph node metastasis (P < 0.05). In contrast, although strong staining of P-Akt occurred in 14 of 44 cases (32%), there was no significant correlation between the positive staining of P-Akt and cytoplasmic β-catenin. Taken together these results suggest that the lost membranous β-catenin might translocate to cytoplasm depending on reduced expression of E-cadherin, while Akt seems unlikely to play a role in this process
Krüppel-like factor 4 represses transcription of the survivin gene in esophageal cancer cell lines
No full textAberrant expression of survivin has been shown to be regulated at the transcription level in cancer cells. In this study, we demonstrate that there are six putative binding sites of Krüppel-like factor 4 (KLF4) within the 2000-bp region upstream of the transcription start site of the human survivin gene. Luciferase reporter gene assays revealed that survivin promoter activity is repressed upon overexpression of KLF4 in EC9706 cells. A chromatin immunoprecipitation assay indicated that KLF4 indeed binds the survivin promoter in vivo. It specifically binds the site located at position -40 among the six binding sites as determined by electrophoretic mobility shift assay. Ectopic expression of KLF4 decreases the mRNA and protein levels of survivin. Furthermore, overexpression of survivin partially reverses KLF4-induced cell apoptosis. These results indicate that KLF4 is a transcriptional repressor of the human survivin gene in esophageal squamous cancer cells
Co-curing bonding of carbon fibre/epoxy composite joints with excellent structure integrity using carbon fibre/PEEK tapes
No full textA novel co-curing process was proposed for the bonding of carbon fibre/epoxy composites by replacing traditional epoxy adhesives with carbon fibre/PEEK (CF/PEEK) tapes, with an attempt to improve the structure integrity. The lap-shear strengths, fatigue resistance and mode-I and mode-II fracture behaviour of the co-cured joints at 22 °C and 130 °C were investigated, and the failure mechanisms were also studied. The experimental results demonstrated that, by replacing an aerospace structural adhesive with surface-treated CF/PEEK tapes for the co-curing bonding of composite joints, the lap-shear strength of the joints had been increased by 47% and 68% at 22 °C and 130 °C, respectively; the fatigue life had been extended by 3.39 times; the mode-I fracture energy had been increased by 70% and 182% at 22 °C and 130 °C, respectively; and the mode-II fracture energy had been increased by 59% and 54% at 22 °C and 130 °C, respectively. An analysis on the failure surfaces of the tested specimens proved significant plastic deformation and breakage of the PEEK resin and extensive carbon fibre delamination being the main failure mechanisms of the CF/PEEK bonded joints. Overall, this study demonstrated a huge potential of replacing traditional film adhesives with CF/PEEK tapes for the co-curing bonding of aerospace composite joints with significantly enhanced structure integrity and thermal stability.Green Open Access added to TU Delft Institutional Repository ‘You share, we take care!’ – Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Structural Integrity & Composite
Affidavit of Florence Scrivner Toye re: transfer of Lease D, Carson Estate Company to Quan Bros., February 25, 1943
No full textDescribes transfer of Lease D with the Carson Estate Company from Florence Scrivner Toye to the Quan Bros. company; Quan Him Wong, George G. Quan. Signatures representing Florence Scrivner Toye, Harry G. Toye, Quan Him Wong, George G. Quan and Hamilton H. Cotton of the Carson Estate Company are included
Overexpression of EB1 in human esophageal squamous cell carcinoma (ESCC) may promote cellular growth by activating β-catenin/TCF pathway
No full textEsophageal squamous cell carcinoma (ESCC) has a multifactorial etiology involving environmental and/or genetic factors. End-binding protein 1 (EB1), which was cloned as an interacting partner of the adenomatous polyposis coli (APC) tumor suppressor protein, was previously found overexpressed in ESCC. However, the precise role of EB1 in the development of this malignancy has not yet been elucidated. In this study, we analysed freshly resected ESCC specimens and demonstrated that EB1 was overexpressed in approximately 63% of tumor samples compared to matched normal tissue. We report that overexpression of EB1 in the ESCC line EC9706 significantly promotes cell growth, whereas suppression of EB1 protein level by RNA interference significantly inhibited growth of esophageal tumor cells. In addition, EB1 overexpression induced nuclear accumulation of β-catenin and promoted the transcriptional activity of β-catenin/T-cell factor (TCF). These effects were partially or completely abolished by coexpression of APC or ΔN TCF4, respectively. Also, we found that EB1 affected the interaction between β-catenin and APC. Furthermore, EB1 overexpression was correlated with cytoplasmic/nuclear accumulation of β-catenin in primary human ESCC. Taken together, these results support the novel hypothesis that EB1 overexpression may play a role in the development of ESCC by affecting APC function and activating the β-catenin/TCF pathway
[Affidavit] of Florence Scrivner Toye re: transfer of Lease D to Quan Bros., Carson Estate Company, January 6, 1943
No full textDescribes transfer of Lease D with the Carson Estate Company from Florence Scrivner Toye to the Quan Bros. company; Quan Him Wong, George G. Quan. No signatures on this document
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