Latest Publications

@article{vondalova_blanarova_cisplatin_2011,

title = {Cisplatin and a potent platinum(IV) complex-mediated enhancement of TRAIL-induced cancer cells killing is associated with modulation of upstream events in the extrinsic apoptotic pathway.},

author = {Olga Vondálová Blanárová and Iva Jelínková and Arpád Szöor and Belma Skender and Karel Soucek and Viktor Horváth and Alena Vaculová and Ladislav Andera and Petr Sova and János Szöllosi and Jirina Hofmanová and György Vereb and Alois Kozubík},

doi = {10.1093/carcin/bgq220},

issn = {1460-2180 0143-3334},

year  = {2011},

date = {2011-01-01},

journal = {Carcinogenesis},

volume = {32},

number = {1},

pages = {42–51},

abstract = {TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) can selectively trigger apoptosis in various cancer cell types. However, many cancer cells are resistant to death receptor-mediated apoptosis. Combination therapy with platinum complexes may affect TRAIL-induced signaling via modulation of various steps in apoptotic pathways. Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used in 20-fold lower concentration enhanced killing effects of TRAIL in human colon and prostate cancer cell lines via stimulation of caspase activity and overall apoptosis. Both platinum complexes increased DR5 surface expression in colon cancer cells. Small interfering RNA-mediated DR5 silencing rescued cells from sensitizing effects of platinum drugs on TRAIL-induced caspase-8 activation and apoptosis, showing the functional importance of DR5 in the effects observed. In addition, both cisplatin and LA-12 triggered the relocalization of DR4 and DR5 receptors to lipid rafts and accelerated internalization of TRAIL, which may also affect TRAIL signaling. Collectively, modulations of the initial steps of the extrinsic apoptotic pathway at the level of DR5 and plasma membrane are important for sensitization of colon and prostate cancer cells to TRAIL-induced apoptosis mediated by LA-12 and cisplatin.},

note = {Place: England},

keywords = {Amantadine/*analogs & derivatives/pharmacology, Apoptosis/*drug effects/physiology, Blotting, Cell Line, Cell Separation, Cisplatin/*pharmacology, Confocal, Flow Cytometry, Fluorescent Antibody Technique, Humans, Microscopy, Neoplasms/*metabolism, Organoplatinum Compounds/*pharmacology, Protein Transport/drug effects, Receptors, Reverse Transcriptase Polymerase Chain Reaction, RNA Interference, Signal Transduction/*drug effects/physiology, TNF-Related Apoptosis-Inducing Ligand/*metabolism, TNF-Related Apoptosis-Inducing Ligand/metabolism, 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}

}