A5021845632- Cancer, Lipids, and Metabolism
- Fatty Acid Research and Health
- Cell death mechanisms and regulation
- Peroxisome Proliferator-Activated Receptors
- Retinoids in leukemia and cellular processes
- NF-κB Signaling Pathways
- Estrogen and related hormone effects
- Inflammatory mediators and NSAID effects
- Metal complexes synthesis and properties
- Eicosanoids and Hypertension Pharmacology
- Cancer, Hypoxia, and Metabolism
- Cytokine Signaling Pathways and Interactions
- Cholesterol and Lipid Metabolism
- Metabolomics and Mass Spectrometry Studies
- Lipid metabolism and biosynthesis
- Cancer-related Molecular Pathways
- Photodynamic Therapy Research Studies
- Mitochondrial Function and Pathology
- Immune Response and Inflammation
- Synthesis and biological activity
- Sphingolipid Metabolism and Signaling
- Glutathione Transferases and Polymorphisms
- Nanoplatforms for cancer theranostics
- Natural product bioactivities and synthesis
- Drug Transport and Resistance Mechanisms
Czech Academy of Sciences, Institute of Biophysics
2012-2021
Masaryk University
2009-2021
Czech Academy of Sciences
2007-2016
University of Debrecen
2006
University of Warsaw
2006
University of Würzburg
2006
University Children's Hospital Tübingen
2006
Temple Street Children's University Hospital
2006
Olgahospital
2006
The effects of the histone deacetylase inhibitors (HDACi) trichostatin A (TSA) and sodium butyrate (NaBt) were studied in A549, HT29 FHC human cell lines. Global hyperacetylation, leading to decondensation interphase chromatin, was characterized by an increase H3(K9) H3(K4) dimethylation acetylation. levels all isoforms heterochromatin protein, HP1, reduced after HDAC inhibition. observed changes protein accompanied their patterns. In control cells, acetylation substantially a thin layer at...
Extracts of sediment samples collected from the Morava River and its tributaries (Czech Republic) were examined for mutagenic, dioxin-like, estrogenic activities. Moreover, human leukemic HL-60 cell line was tested as a potential model detection effects environmental contaminants on proliferation differentiation processes. Analytical data indicate that sediments contaminated predominantly with polycyclic aromatic hydrocarbons (PAHs) phthalate esters. The sums concentrations 16 U.S....
The development of colon cancer, one the most common malignancies, is accompanied with numerous lipid alterations. However, analyses whole tumor samples may not always provide an accurate description specific changes occurring directly in epithelial cells. Here, we analyzed detail phospholipid (PL), lysophospholipid (lysoPL), and fatty acid (FA) profiles purified EpCAM+ cells, isolated from adjacent non-tumor tissues cancer patients. We found that a number FAs increased significantly which...
TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) can selectively trigger apoptosis in various cancer cell types. However, many cells are resistant to death receptor-mediated apoptosis. Combination therapy with platinum complexes may affect TRAIL-induced signaling via modulation of steps apoptotic pathways. Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used 20-fold lower concentration enhanced killing effects human colon and prostate lines stimulation...
Abstract We verified the hypothesis suggesting modulation of effects sodium butyrate (NaBt) by ω–3 or ω–6 PUFAs. Comparing response human colon epithelial cell lines fetal (FHC) and adenocarcinoma (HT‐29, HCT‐116) origin, we detected significant differences in proliferation, differentiation apoptotic to treatment NaBt, arachidonic docosahexaenoic acids their combination. While FHC HT‐29 cells NaBt induced G0/G1 arrest, low level apoptosis, HCT‐116 G2/M no high degree apoptosis were detected....
Epithelial cells can be manipulated to undergo apoptosis depending on the balance between pro‐survival and apoptotic signals. We showed that TRAIL‐induced may differentially regulated by inhibitors of MEK ERK (U0126) or PI3K/Akt (LY294002) pathway in TRAIL‐sensitive (HT‐29) TRAIL‐resistant (SW620) human epithelial colon cancer cells. U0126 LY294002 significantly enhanced HT–29 cells, but not SW620 report a different regulation level an anti‐apoptotic Mcl‐1 protein under MEK/ERK inhibition...
Abstract One proposal to increase the efficiency of photodynamic therapy (PDT) is accompany photosensitization with other treatment modalities, including modulation arachidonic acid (AA) metabolism. The aim this study was evaluate effectiveness a combined modality approach employing 48 and 24 h pretreatment various inhibitors lipoxygenase (LOX; nordihydroguaiaretic acid, esculetin, AA‐861, MK‐886 baicalein), cyclooxygenase (COX; diclofenac, flurbiprofen, ibuprofen, indomethacin, SC‐560...
Identification of changes phospholipid (PL) composition occurring during colorectal cancer (CRC) development may help us to better understand their roles in CRC cells. Here, we used LC-MS/MS-based PL profiling cell lines derived from normal colon mucosa, or isolated at distinct stages development, order study alterations species potentially linked with transformation. We found that a detailed evaluation phosphatidylinositol (PI) and phosphatidylserine (PS) classes allowed cluster the studied...
Abstract Differentiating myeloid cells may become resistant to various apoptotic stimuli. In the present study, dimethyl sulfoxide (DMSO) and all-trans retinoic acid (ATRA) were found modulate sensitivity of HL-60 death receptor-mediated apoptosis in a time-dependent manner. During early stages differentiation, DMSO treatment increased response tumor necrosis factor α; (TNF-α), but enhanced responsiveness was lost during later differentiation stages. contrast, ATRA induced resistance...