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    The Role of Bcl-2 and Beclin-1 Complex in “Switching” between Apoptosis and Autophagy in Human Glioma Cells upon LY294002 and Sorafenib Treatment

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    cells-12-02670.pdf (7.963MB)
    Data
    2023
    Autor
    Zająć, Adrian
    Maciejczyk, Aleksandra
    Sumorek-Wiadro, Joanna
    Filipek, Karol
    Deryło, Kamil
    Langner, Ewa
    Pawelec, Jarosław
    Wasiak, Magdalena
    Ścibiorski, Mateusz
    Rzeski, Wojciech
    Tchórzewski, Marek
    Reichert, Michał
    Joanna Jakubowicz-Gil, Joanna
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    Streszczenie
    Background: Gliomas are the most malignant tumors of the central nervous system. One of the factors in their high drug resistance is avoiding programmed death (PCD) induction. This is related to the overexpression of intracellular survival pathways: PI3K-Akt/PKB-mTOR and Ras-Raf-MEK-ERK. Apoptosis and autophagy are co-existing processes due to the interactions between Bcl-2 and beclin-1 proteins. Their complex may be a molecular “toggle-switch” between PCD types. The aim of this research was to investigate the role of Bcl-2:beclin-1 complex in glioma cell elimination through the combined action of LY294002 and sorafenib. Methods: Drug cytotoxicity was estimated with an MTT test. The type of cell death was evaluated using variant microscopy techniques (fluorochrome staining, immunocytochemistry, and transmission electron microscopy), as well as the Bcl-2:beclin-1 complex formation and protein localization. Molecular analysis of PCD indicators was conducted through immunoblotting, immunoprecipitation, and ELISA testing. SiRNA was used to block Bcl-2 and beclin-1 expression. Results: The results showed the inhibitors used in simultaneous application resulted in Bcl-2:beclin-1 complex formation and apoptosis becoming dominant. This was accompanied by changes in the location of the tested proteins. Conclusions: “Switching” between apoptosis and autophagy using PI3K and Raf inhibitors with Bcl-2:beclin-1 complex formation opens new therapeutic perspectives against gliomas.
    URI
    https://www.mdpi.com/2073-4409/12/23/2670
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    DSpace software copyright © 2002-2016  DuraSpace
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