Latest Publications

@article{takacova_role_2009,

title = {Role of aryl hydrocarbon receptor in modulation of the expression of the hypoxia marker carbonic anhydrase IX.},

author = {Martina Takacova and Tereza Holotnakova and Jan Vondracek and Miroslav Machala and Katerina Pencikova and Katarina Gradin and Lorenz Poellinger and Jaromir Pastorek and Silvia Pastorekova and Juraj Kopacek},

doi = {10.1042/BJ20080952},

issn = {1470-8728 0264-6021},

year  = {2009},

date = {2009-04-01},

journal = {The Biochemical journal},

volume = {419},

number = {2},

pages = {419–425},

abstract = {Tumour-associated expression of CA IX (carbonic anhydrase IX) is to a major extent regulated by HIF-1 (hypoxia-inducible factor-1) which is important for transcriptional activation and consists of the oxygen-regulated subunit HIF-1alpha and the partner factor ARNT [AhR (aryl hydrocarbon receptor) nuclear translocator]. We have previously observed that HIF-1alpha competes with the AhR for interaction with ARNT under conditions when both conditionally regulated factors are activated. We have therefore investigated whether TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin)-induced activation of the AhR pathway might interfere with CA IX expression. The results from the present study suggest that TCDD treatment reduces hypoxic induction of both CA IX mRNA and protein expression. Moreover, the transcriptional activity of the CA9 promoter was significantly reduced by expression of CAAhR (constitutively active AhR), which activates transcription in a ligand-independent manner. Finally, we found that ARNT is critical for both hypoxic induction and the TCDD-mediated inhibition of CA9 expression.},

note = {Place: England},

keywords = {alpha Subunit, Animals, Antigens, Aryl Hydrocarbon/genetics/metabolism/*physiology, Binding Sites, Blotting, Carbonic Anhydrase IX, Carbonic Anhydrases/genetics/*metabolism, Cell Hypoxia/genetics/*physiology, Cell Line, Chromatin Immunoprecipitation, Genetic/genetics, Humans, Hypoxia-Inducible Factor 1, Mice, Neoplasm/genetics, Polychlorinated Dibenzodioxins/pharmacology, Polymerase Chain Reaction, Promoter Regions, Protein Binding/drug effects, Receptors, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction/drug effects, Tumor, Western},

pubstate = {published},

tppubtype = {article}

}

@article{maioli_rottlerin_2009,

title = {Rottlerin inhibits ROS formation and prevents NFkappaB activation in MCF-7 and HT-29 cells.},

author = {Emanuela Maioli and Lucedio Greci and Karel Soucek and Martina Hyzdalova and Alessandra Pecorelli and Vittoria Fortino and Giuseppe Valacchi},

doi = {10.1155/2009/742936},

issn = {1110-7251 1110-7243},

year  = {2009},

date = {2009-01-01},

journal = {Journal of biomedicine & biotechnology},

volume = {2009},

pages = {742936},

abstract = {Rottlerin, a polyphenol isolated from Mallotus Philippinensis, has been recently used as a selective inhibitor of PKC delta, although it can inhibit many kinases and has several biological effects. Among them, we recently found that Rottlerin inhibits the Nuclear Factor kappaB (NFkappaB), activated by either phorbol esters or H(2)O(2). Because of the redox sensitivity of NFkappaB and on the basis of Rottlerin antioxidant property, we hypothesized that Rottlerin could prevent NFkappaB activation acting as a free radicals scavenger, as other natural polyphenols. The current study confirms the antioxidant property of Rottlerin against the 2,2-diphenyl-1-picrylhydrazyl radical (DPPH) in vitro and against oxidative stress induced by H(2)O(2) and by menadione in culture cells. We also demonstrate that Rottlerin prevents TNFalpha-dependent NFkappaB activation in MCF-7 cells and in HT-29 cells transfected with the NFkappaB-driven plasmid pBIIX-LUC, suggesting that Rottlerin can inhibit NFkappaB via several pathways and in several cell types.},

note = {Place: United States},

keywords = {Acetophenones/chemistry/*pharmacology, Benzopyrans/chemistry/*pharmacology, Biphenyl Compounds/metabolism, Cell Nucleus/drug effects/metabolism, DNA/metabolism, Electron Spin Resonance Spectroscopy, Free Radical Scavengers/pharmacology, Genetic/drug effects, HT29 Cells, Humans, Hydrogen Peroxide/metabolism, Intracellular Space/drug effects/metabolism, NF-kappa B/*metabolism, Picrates/metabolism, Protein Binding/drug effects, Protein Transport/drug effects, Reactive Oxygen Species/*metabolism, Spectrophotometry, Transcription, Transfection, Tumor Necrosis Factor-alpha/pharmacology, Ultraviolet},

pubstate = {published},

tppubtype = {article}

}