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alpha-tocopheryl succinate-induced apoptosis in human gastric cancer cells is modulated by ERK1/2 and c-Jun N-terminal kinase in a biphasic manner

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F07%3A00097145" target="_blank" >RIV/68378050:_____/07:00097145 - isvavai.cz</a>

  • Result on the web

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    alpha-tocopheryl succinate-induced apoptosis in human gastric cancer cells is modulated by ERK1/2 and c-Jun N-terminal kinase in a biphasic manner

  • Original language description

    Stomach cancer is the frequent cause of cancer-related deaths with poor prognosis. Here we studied the effect of ? tocopheryl succinate (? TOS ) on the gastric cancer cell line SGC-7901. ? TOS inhibited proliferation of the cells and induced their apoptosis in a concentration- and time-dependent manner, while ?-tocopherol showed no effect. The effect of ? TOS was modulated by components of the MAPK signaling network, including ERK1/2 and c-Jun N-terminal kinase (JNK), but not p38. Activation of ERK1/2 occurred early and increased until 12 h, coinciding with an increase in apoptosis, then it dropped abruptly, while activation of JNK rose steadily, reaching a plateau at 12 h of ? TOS treatment. The effects of ERK1/2 and JNK on the apoptosis outcome are transmitted via c-Jun, since transfection of the cells with c-Jun antisense oligodeoxynucleotide inhibited ? TOS-induced apoptosis. We conclude that ERK1/2 and JNK positively regulate apoptosis induced in gastric cancer cells by ? TOS.

  • Czech name

    Apoptóza indukovaná alfa-tokoferylsukcinátem v buňkách rakoviny žaludku je modulována proteinkinázami ERK1/2 a c-Jun bifázickým způsobem

  • Czech description

    Rakovina žaludku je velmi častou příčinou úmrtí a má špatnou prognózu. Studovali jsme vliv ? tokoferylsukcinátu na linii buněk rakoviny žaludku SGC-7901. ? TOS inhiboval dělení buněk a indukoval jejich apoptózu způsobem závislým na koncentraci a čase, zatímco ?-tokoferol nevykazoval žádný vliv. Složky MAPK signální sítě, včetně proteinkináz ERK1/2 a N-konce c-Jun (JNK), nikoliv však p38, modulovaly vliv ? TOS. Aktivace ERK1/2 nastávala časně a zvyšovala se do 12. h; koincidovala tak se vzestupem apoptózy a pak náhle poklesla. Aktivace JNK vzrůstala rovnoměrně s ustálením ve 12. h působení ? TOS. Vlivy ERK1/2 a JNK na výslednou apoptózu jsou zprostředkovány c-Jun, jak vyplývá z transfekce buněk c-Jun antisense oligodeoxynukleotidem vedoucí k inhibici apoptózy indukované ? TOS. Závěrem lze říci, že ERK1/2 a JNK pozitivně regulují apoptózu indukovanou v buňkách rakoviny žaludku ? TOS.

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    EB - Genetics and molecular biology

  • OECD FORD branch

Result continuities

  • Project

  • Continuities

    Z - Vyzkumny zamer (s odkazem do CEZ)

Others

  • Publication year

    2007

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Cancer letters

  • ISSN

    0304-3835

  • e-ISSN

  • Volume of the periodical

    247

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    NL - THE KINGDOM OF THE NETHERLANDS

  • Number of pages

    8

  • Pages from-to

    345-352

  • UT code for WoS article

  • EID of the result in the Scopus database