کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8260692 | 1534665 | 2013 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Negative modulation of mitochondrial oxidative phosphorylation by epigallocatechin-3 gallate leads to growth arrest and apoptosis in human malignant pleural mesothelioma cells
ترجمه فارسی عنوان
مدولاسیون منفی فسفوریلاسیون اکسیداتیو میتوکندری توسط اپیمالاکا تکتین 3 گالات منجر به توقف رشد و آپوپتوز در سلول های مزوتلیوم بدخیم انسان می شود
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کلمات کلیدی
MALSuccXTTCyt CdichlorofluoresceinMRCEpigallocatechin-3-gallateDCFH-DAMMESTAT3OXPHOSEGCGDcfCAT2′,7′-dichlorofluorescein diacetate - 2 '، 7'-dichlorofluorescein diacetateROS - ROSMitochondrial respiratory chain - زنجیره تنفسی mitochondrialSOD - سدSuperoxide dismutase - سوکسوکس دیسموتازSuccinate - سوکینتینcytochrome c - سیتوکروم سیOxidative phosphorylation - فسفوریلاسیون اکسیداتیوmalate - مالتMalignant mesothelioma - مزوتلیوما بدخیمMitochondria - میتوکندریاCatalase - کاتالازGlu - گلوglutamate - گلوتاماتReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Increasing evidence reveals a large dependency of epithelial cancer cells on oxidative phosphorylation (OXPHOS) for energy production. In this study we tested the potential of epigallocatechin-3-gallate (EGCG), a natural polyphenol known to target mitochondria, in inducing OXPHOS impairment and cell energy deficit in human epitheliod (REN cells) and biphasic (MSTO-211H cells) malignant pleural mesothelioma (MMe), a rare but highly aggressive tumor with high unmet need for treatment. Due to EGCG instability that causes H2O2 formation in culture medium, the drug was added to MMe cells in the presence of exogenous superoxide dismutase and catalase, already proved to stabilize the EGCG molecule and prevent EGCG-dependent reactive oxygen species formation. We show that under these experimental conditions, EGCG causes the selective arrest of MMe cell growth with respect to normal mesothelial cells and the induction of mitochondria-mediated apoptosis, as revealed by early mitochondrial ultrastructure modification, swelling and cytochrome c release. We disclose a novel mechanism by which EGCG induces apoptosis through the impairment of mitochondrial respiratory chain complexes, particularly of complex I, II and ATP synthase. This induces a strong reduction in ATP production by OXPHOS, that is not adequately counterbalanced by glycolytic shift, resulting in cell energy deficit, cell cycle arrest and apoptosis. The EGCG-dependent negative modulation of mitochondrial energy metabolism, selective for cancer cells, gives an important input for the development of novel pharmacological strategies for MMe.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1832, Issue 12, December 2013, Pages 2085-2096
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1832, Issue 12, December 2013, Pages 2085-2096
نویسندگان
Daniela Valenti, Lidia de Bari, Gabriella Arcangela Manente, Leonardo Rossi, Luciano Mutti, Laura Moro, Rosa Anna Vacca,