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Loss of PTEN Facilitates Rosiglitazone-Mediated Enhancement of Platinum(IV) Complex LA-12-Induced Apoptosis in Colon Cancer Cells

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F15%3A00452062" target="_blank" >RIV/68081707:_____/15:00452062 - isvavai.cz</a>

  • Alternative codes found

    RIV/00179906:_____/15:10314407 RIV/00216224:14310/15:00095868

  • Result on the web

    <a href="http://dx.doi.org/10.1371/journal.pone.0141020" target="_blank" >http://dx.doi.org/10.1371/journal.pone.0141020</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1371/journal.pone.0141020" target="_blank" >10.1371/journal.pone.0141020</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Loss of PTEN Facilitates Rosiglitazone-Mediated Enhancement of Platinum(IV) Complex LA-12-Induced Apoptosis in Colon Cancer Cells

  • Original language description

    We demonstrated for the first time an outstanding ability of rosiglitazone to mediate a profound enhancement of LA-12-induced apoptosis associated with activation of mitochondrial pathway in human colon cancer cells. This effect was preferentially observed in the G1 cell cycle phase, independent on p53 and PPAR. proteins, and accompanied with significant changes of selected Bcl-2 family protein levels. Further stimulation of cooperative synergic cytotoxic action of rosiglitazone and LA-12 was demonstrated in the cells deficient for PTEN, where mitochondrial apoptotic pathway was more stimulated and G1-phase-associated dying was reinforced. Our results suggest that combined treatment with rosiglitazone and LA-12 might be promising anticancer strategy incolon-derived tumours regardless of their p53 status, and also favourable in those defective in PTEN function.

  • Czech name

  • Czech description

Classification

  • Type

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

  • CEP classification

    BO - Biophysics

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/GA15-06650S" target="_blank" >GA15-06650S: Novel molecular mechanisms involved in chemotherapeutic drug- and cytokine-induced cancer cell death</a><br>

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2015

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    PLoS ONE

  • ISSN

    1932-6203

  • e-ISSN

  • Volume of the periodical

    10

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    20

  • Pages from-to

  • UT code for WoS article

    000363249300023

  • EID of the result in the Scopus database