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Shihai Yang - One of the best experts on this subject based on the ideXlab platform.
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Vanillic Acid suppresses hif 1α expression via inhibition of mtor p70s6k 4e bp1 and raf mek erk pathways in human colon cancer hct116 cells
International Journal of Molecular Sciences, 2019Co-Authors: Jingli Gong, Shengxue Zhou, Shihai YangAbstract:Hypoxia-inducible factor 1 (HIF-1) plays a pivotal role in tumor adaptation to microenvironmental hypoxia, and it also exerts important roles in angiogenesis and tumor development. Vanillic Acid is a dietary phenolic compound reported to exhibit anticancer properties. However, the mechanisms by which Vanillic Acid inhibits tumor growth are not fully understood. Here, we investigated the effect of Vanillic Acid on HIF-1α activation. Vanillic Acid significantly inhibits HIF-1α expression induced by hypoxia in various human cancer cell lines. Further analysis revealed that Vanillic Acid inhibited HIF-1α protein synthesis. Neither the HIF-1α protein degradation rate nor the steady-state HIF-1α mRNA levels were affected by Vanillic Acid. Moreover, Vanillic Acid inhibited HIF-1α expression by suppressing mammalian target of rapamycin/p70 ribosomal protein S6 kinase/eukaryotic initiation factor 4E-binding protein-1 and Raf/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK pathways. We found that Vanillic Acid dose-dependently inhibited VEGF and EPO protein expressions and disrupted tube formation. The results suggest that Vanillic Acid effectively inhibits angiogenesis. Flow cytometry analysis demonstrated that Vanillic Acid significantly induced G1 phase arrest and inhibited the proliferation of human colon cancer HCT116 cells. In vivo experiments confirmed that Vanillic Acid treatment caused significant inhibition of tumor growth in a xenografted tumor model. These studies reveal that Vanillic Acid is an effective inhibitor of HIF-1α and provides new perspectives into the mechanism of its antitumor activity.
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Vanillic Acid Suppresses HIF-1α Expression via Inhibition of mTOR/p70S6K/4E-BP1 and Raf/MEK/ERK Pathways in Human Colon Cancer HCT116 Cells
MDPI AG, 2019Co-Authors: Jingli Gong, Shengxue Zhou, Shihai YangAbstract:Hypoxia-inducible factor 1 (HIF-1) plays a pivotal role in tumor adaptation to microenvironmental hypoxia, and it also exerts important roles in angiogenesis and tumor development. Vanillic Acid is a dietary phenolic compound reported to exhibit anticancer properties. However, the mechanisms by which Vanillic Acid inhibits tumor growth are not fully understood. Here, we investigated the effect of Vanillic Acid on HIF-1α activation. Vanillic Acid significantly inhibits HIF-1α expression induced by hypoxia in various human cancer cell lines. Further analysis revealed that Vanillic Acid inhibited HIF-1α protein synthesis. Neither the HIF-1α protein degradation rate nor the steady-state HIF-1α mRNA levels were affected by Vanillic Acid. Moreover, Vanillic Acid inhibited HIF-1α expression by suppressing mammalian target of rapamycin/p70 ribosomal protein S6 kinase/eukaryotic initiation factor 4E-binding protein-1 and Raf/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK pathways. We found that Vanillic Acid dose-dependently inhibited VEGF and EPO protein expressions and disrupted tube formation. The results suggest that Vanillic Acid effectively inhibits angiogenesis. Flow cytometry analysis demonstrated that Vanillic Acid significantly induced G1 phase arrest and inhibited the proliferation of human colon cancer HCT116 cells. In vivo experiments confirmed that Vanillic Acid treatment caused significant inhibition of tumor growth in a xenografted tumor model. These studies reveal that Vanillic Acid is an effective inhibitor of HIF-1α and provides new perspectives into the mechanism of its antitumor activity
Marcel Asther - One of the best experts on this subject based on the ideXlab platform.
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Design of a fungal bioprocess for vanillin production from Vanillic Acid at scalable level by Pycnoporus cinnabarinus
Journal of bioscience and bioengineering, 2000Co-Authors: Christelle Stentelaire, Benoit Colonna Ceccaldi, Laurence Lesage-meessen, Olivier Bernard, Georges Bastin, Julie Oddou, Marcel AstherAbstract:The biotechnological process of vanillin production from Vanillic Acid by Pycnoporus cinnabarinus was scaled-up at the laboratory level. Vanillin production was studied in two types of bioreactors, a mechanically agitated and an air-lift bioreactor. In the mechanically agitated bioreactor where vanillin was produced in greater quantities, oxygen availability was studied during the growth and production phases. A maximal aeration rate (90l/h equivalent to 0.83 volume of air/volume of medium/min or vvm) during the growth phase and a minimal aeration rate (30 l/h equivalent to 0.28 vvm) during the production phase were necessary to increase vanillin production to 1260 mg/l. Vanillic Acid bioconversion to vanillin occurred under the conditions of reduced dissolved oxygen concentration, gentle agitation, high carbon dioxide production and low specific growth rate. However, under these conditions, vanillin production was accompanied by a significant amount of methoxyhydroquinone. Vanillin over a concentration of 1000 mg/l was shown to be highly toxic to the growth of P. cinnabarinus on agar medium. The application of selective XAD-2 resin led to a reduction of vanillin concentration in the medium, thus limiting its toxicity towards the fungal biomass as well as the formation of unwanted by-products such as methoxyhydroquinone and allowed the concentration of vanillin produced to reach 1575 mg/l.
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Mass balance modeling of vanillin production from Vanillic Acid by cultures of the fungus Pycnoporus cinnabarinus in bioreactors
Biotechnology and bioengineering, 1999Co-Authors: Olivier Bernard, Christelle Stentelaire, Laurence Lesage-meessen, Georges Bastin, Marcel AstherAbstract:A systematic two-step procedure for the structural identification of bioprocesses is followed in order to establish a mechanistic model for vanillin production by Pycnoporus cinnabarinus. The first step is devoted to the identification of the underlying reaction structure and the development of a validated mass balance model for the growth of P. cinnabarinus and the biotransformation of Vanillic Acid into vanillin. The second step is devoted to the kinetic modeling, namely, the estimation of the reaction rates and the calibration of the kinetic parameters. The whole procedure leads to the final set up of a simulation model of the process. The results are supported by the data from five cultures of P. cinnabarinus in bioreactors. (C) 1999 John Wiley & Sons, Inc.
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An attempt to channel the transformation of Vanillic Acid into vanillin by controlling methoxyhydroquinone formation in Pycnoporus cinnabarinus with cellobiose
Applied Microbiology and Biotechnology, 1997Co-Authors: Laurence Lesage-meessen, Mireille Haon, M. Delattre, J.f. Thibault, B. Colonna Ceccaldi, Marcel AstherAbstract:The effects of adding cellobiose on the transformation of Vanillic Acid to vanillin by two strains of Pycnoporus cinnabarinus MUCL39532 and MUCL38467 were studied. When maltose was used as the carbon source in the culture medium, very high levels of methoxyhydroquinone were formed from Vanillic Acid. When cellobiose was used as the carbon source and/or added to the culture medium of P. cinnabarinus strains on day 3 just before Vanillic Acid was added, it channelled the Vanillic Acid metabolism via the reductive route leading to vanillin. Adding 3.5 g l−1 cellobiose to 3-day-old maltose cultures of P. cinnabarinus MUCL39532 and 2.5 g l−1 cellobiose to 3-day-old cellobiose cultures of P. cinnabarinus MUCL38467, yielded 510 mg l−1 and 560 mg l−1 vanillin with a molar yield of 50.2 % and 51.7 % respectively. Cellobiose may either have acted as an easily metabolizable carbon source, required for the reductive pathway to occur, or as an inducer of cellobiose:quinone oxidoreductase, which is known to inhibit Vanillic Acid decarboxylation.
Jingli Gong - One of the best experts on this subject based on the ideXlab platform.
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Vanillic Acid suppresses hif 1α expression via inhibition of mtor p70s6k 4e bp1 and raf mek erk pathways in human colon cancer hct116 cells
International Journal of Molecular Sciences, 2019Co-Authors: Jingli Gong, Shengxue Zhou, Shihai YangAbstract:Hypoxia-inducible factor 1 (HIF-1) plays a pivotal role in tumor adaptation to microenvironmental hypoxia, and it also exerts important roles in angiogenesis and tumor development. Vanillic Acid is a dietary phenolic compound reported to exhibit anticancer properties. However, the mechanisms by which Vanillic Acid inhibits tumor growth are not fully understood. Here, we investigated the effect of Vanillic Acid on HIF-1α activation. Vanillic Acid significantly inhibits HIF-1α expression induced by hypoxia in various human cancer cell lines. Further analysis revealed that Vanillic Acid inhibited HIF-1α protein synthesis. Neither the HIF-1α protein degradation rate nor the steady-state HIF-1α mRNA levels were affected by Vanillic Acid. Moreover, Vanillic Acid inhibited HIF-1α expression by suppressing mammalian target of rapamycin/p70 ribosomal protein S6 kinase/eukaryotic initiation factor 4E-binding protein-1 and Raf/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK pathways. We found that Vanillic Acid dose-dependently inhibited VEGF and EPO protein expressions and disrupted tube formation. The results suggest that Vanillic Acid effectively inhibits angiogenesis. Flow cytometry analysis demonstrated that Vanillic Acid significantly induced G1 phase arrest and inhibited the proliferation of human colon cancer HCT116 cells. In vivo experiments confirmed that Vanillic Acid treatment caused significant inhibition of tumor growth in a xenografted tumor model. These studies reveal that Vanillic Acid is an effective inhibitor of HIF-1α and provides new perspectives into the mechanism of its antitumor activity.
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Vanillic Acid Suppresses HIF-1α Expression via Inhibition of mTOR/p70S6K/4E-BP1 and Raf/MEK/ERK Pathways in Human Colon Cancer HCT116 Cells
MDPI AG, 2019Co-Authors: Jingli Gong, Shengxue Zhou, Shihai YangAbstract:Hypoxia-inducible factor 1 (HIF-1) plays a pivotal role in tumor adaptation to microenvironmental hypoxia, and it also exerts important roles in angiogenesis and tumor development. Vanillic Acid is a dietary phenolic compound reported to exhibit anticancer properties. However, the mechanisms by which Vanillic Acid inhibits tumor growth are not fully understood. Here, we investigated the effect of Vanillic Acid on HIF-1α activation. Vanillic Acid significantly inhibits HIF-1α expression induced by hypoxia in various human cancer cell lines. Further analysis revealed that Vanillic Acid inhibited HIF-1α protein synthesis. Neither the HIF-1α protein degradation rate nor the steady-state HIF-1α mRNA levels were affected by Vanillic Acid. Moreover, Vanillic Acid inhibited HIF-1α expression by suppressing mammalian target of rapamycin/p70 ribosomal protein S6 kinase/eukaryotic initiation factor 4E-binding protein-1 and Raf/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK pathways. We found that Vanillic Acid dose-dependently inhibited VEGF and EPO protein expressions and disrupted tube formation. The results suggest that Vanillic Acid effectively inhibits angiogenesis. Flow cytometry analysis demonstrated that Vanillic Acid significantly induced G1 phase arrest and inhibited the proliferation of human colon cancer HCT116 cells. In vivo experiments confirmed that Vanillic Acid treatment caused significant inhibition of tumor growth in a xenografted tumor model. These studies reveal that Vanillic Acid is an effective inhibitor of HIF-1α and provides new perspectives into the mechanism of its antitumor activity
Cletus J M Dsouza - One of the best experts on this subject based on the ideXlab platform.
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Vanillic Acid as a novel specific inhibitor of snake venom 5 nucleotidase a pharmacological tool in evaluating the role of the enzyme in snake envenomation
Biochemistry, 2009Co-Authors: B L Dhananjaya, A Nataraju, C Raghavendra D Gowda, B K Sharath, Cletus J M DsouzaAbstract:Vanillic Acid has been investigated for its inhibitory effect on Naja naja, Daboia russellii, and Trimeresurus malabaricus venom 5′-nucleotidase activity. Trimeresurus malabaricus venom 5′-nucleotidase activity was 1.3- and 8.0-fold higher than that of N. naja and D. russellii venoms, respectively. Substrate specificity studies showed that for all the venoms tested, 5′-AMP was the preferred substrate for 5′-nucleotidase. This indicates the central role of adenosine in snake envenomation. Vanillic Acid selectively and specifically inhibited 5′-nucleotidase activity among several enzymes present in the three venoms tested. The inhibitor was competitive, as the inhibition was relieved by increased substrate concentration. It appears that the COOH group in Vanillic Acid is the determining factor for inhibition as vanillin, a structurally similar compound with respect to Vanillic Acid, had no inhibitory activity. This study for the first time exemplifies Vanillic Acid as a pharmacological tool in evaluating the role of 5′-nucleotidase in snake envenomation.
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anticoagulant effect of naja naja venom 5 nucleotidase demonstration through the use of novel specific inhibitor Vanillic Acid
Toxicon, 2006Co-Authors: B L Dhananjaya, A Nataraju, C Raghavendra D Gowda, B K Sharath, B S Vishwanath, R Rajesh, Cletus J M DsouzaAbstract:The snake venom proteins affect hemostasis by either advancing/delaying blood coagulation. Apart from proteases and phospholipase A(2)s (PLA(2)s), 5'nucleotidase is known to affect hemostasis by inhibiting platelet aggregation. In this study, the possible involvement of Naja naja venom 5'nucleotidase in mediating anticoagulant affect is evaluated. Vanillic Acid selectively and specifically inhibited 5'nucleotidase activity among other enzymes present in N. naja venom. It is a competitive inhibitor as evident of inhibition relieving upon increased substrate concentration. Vanillic Acid dose dependently inhibited the anticoagulant effect of N. naja venom up to 40%. This partial involvement of 5'nucleotidase in mediating anticoagulant effect is substantiated by concanavalin-A (Con-A) inhibition studies. Con-A, competitively inhibited in vitro protease and 5'nucleotidase activity up to 100%. However, it did not exhibit inhibitory activity on PLA(2). The complete inhibition of anticoagulant effect by Con-A upon recalcification time suggests the participation of both 5'nucleotidase and protease in mediating anticoagulant effect of N. naja venom. Vanillic Acid and Con-A inhibition studies together suggest that probably 5'nucleotidase interacts with one or more factors of intrinsic pathway of blood coagulation to bring about anticoagulant effect. Thus, this study for the first time demonstrates the involvement of 5'nucleotidase in mediating N. naja venom anticoagulant effect.
Eric S Saltzman - One of the best experts on this subject based on the ideXlab platform.
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burning derived Vanillic Acid in an arctic ice core from tunu northeastern greenland
Climate of The Past, 2018Co-Authors: Mackenzie M Grieman, Murat Aydin, Joseph R Mcconnell, Eric S SaltzmanAbstract:Abstract. In this study, Vanillic Acid was measured in the Tunu ice core from northeastern Greenland in samples covering the past 1700 years. Vanillic Acid is an aerosol-borne aromatic methoxy Acid, produced by the combustion of lignin during biomass burning. Air mass trajectory analysis indicates that North American boreal forests are likely the major source region for biomass burning aerosols deposited to the ice core site. Vanillic Acid levels in the Tunu ice core range from
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a method for analysis of Vanillic Acid in polar ice cores
Climate of The Past, 2015Co-Authors: Mackenzie M Grieman, J Greaves, Eric S SaltzmanAbstract:Abstract. Biomass burning generates a wide range of organic compounds that are transported via aerosols to the polar ice sheets. Vanillic Acid is a product of conifer lignin combustion, which has previously been observed in laboratory and ambient biomass burning aerosols. In this study a method was developed for analysis of Vanillic Acid in melted polar ice core samples. Vanillic Acid was chromatographically separated using reversed-phase liquid chromatography (HPLC) and detected using electrospray ionization–triple quadrupole mass spectrometry (ESI-MS/MS). Using a 100 μL injection loop and analysis time of 4 min, we obtained a detection limit of 77 ppt (parts per trillion by mass) and an analytical precision of ±10%. Measurements of Vanillic Acid in Arctic ice core samples from the Siberian Akademii Nauk core are shown as an example application of the method.