RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell death
Abstract The formulation of quercetin nanoliposomes (QUE-NLs) has been shown to enhance QUE antitumor activity in C6 glioma cells. At high concentrations, QUE-NLs induce necrotic cell death. In this study, we probed the molecular mechanisms of QUE-NL-induced C6 glioma cell death and examined whether...
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2013-08-01
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| Series: | Cell Death and Disease |
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| Online Access: | https://doi.org/10.1038/cddis.2013.242 |
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| author | G Wang J J Wang X L Chen S M Du D S Li Z J Pei H Lan L B Wu |
| author_facet | G Wang J J Wang X L Chen S M Du D S Li Z J Pei H Lan L B Wu |
| author_sort | G Wang |
| collection | DOAJ |
| description | Abstract The formulation of quercetin nanoliposomes (QUE-NLs) has been shown to enhance QUE antitumor activity in C6 glioma cells. At high concentrations, QUE-NLs induce necrotic cell death. In this study, we probed the molecular mechanisms of QUE-NL-induced C6 glioma cell death and examined whether QUE-NL-induced programmed cell death involved Bcl-2 family and mitochondrial pathway through STAT3 signal transduction pathway. Downregulation of Bcl-2 and the overexpression of Bax by QUE-NL supported the involvement of Bcl-2 family proteins upstream of C6 glioma cell death. In addition, the activation of JAK2 and STAT3 were altered following exposure to QUE-NLs in C6 glioma cells, suggesting that QUE-NLs downregulated Bcl-2 mRNAs expression and enhanced the expression of mitochondrial mRNAs through STAT3-mediated signaling pathways either via direct or indirect mechanisms. There are several components such as ROS, mitochondrial, and Bcl-2 family shared by the necrotic and apoptotic pathways. Our studies indicate that the signaling cross point of the mitochondrial pathway and the JAK2/STAT3 signaling pathway in C6 glioma cell death is modulated by QUE-NLs. In conclusion, regulation of JAK2/STAT3 and ROS-mediated mitochondrial pathway agonists alone or in combination with treatment by QUE-NLs could be a more effective method of treating chemical-resistant glioma. |
| format | Article |
| id | doaj-art-9e32e962f2bc40e8a7d7af22387aa296 |
| institution | OA Journals |
| issn | 2041-4889 |
| language | English |
| publishDate | 2013-08-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Cell Death and Disease |
| spelling | doaj-art-9e32e962f2bc40e8a7d7af22387aa2962025-08-20T02:27:06ZengNature Publishing GroupCell Death and Disease2041-48892013-08-0148e746e74610.1038/cddis.2013.242RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell deathG Wang0J J Wang1X L Chen2S M Du3D S Li4Z J Pei5H Lan6L B Wu7Department of Pharmacy, Taihe Hospital, Hubei University of MedicineDepartment of Pharmacy, Taihe Hospital, Hubei University of MedicineHubei Provincial Key Laboratory of Embryo Stem CellsDepartment of Pharmacy, Taihe Hospital, Hubei University of MedicineHubei Provincial Key Laboratory of Embryo Stem CellsHubei Provincial Key Laboratory of Embryo Stem CellsDepartment of Pharmacy, Taihe Hospital, Hubei University of MedicineHubei Provincial Key Laboratory of Embryo Stem CellsAbstract The formulation of quercetin nanoliposomes (QUE-NLs) has been shown to enhance QUE antitumor activity in C6 glioma cells. At high concentrations, QUE-NLs induce necrotic cell death. In this study, we probed the molecular mechanisms of QUE-NL-induced C6 glioma cell death and examined whether QUE-NL-induced programmed cell death involved Bcl-2 family and mitochondrial pathway through STAT3 signal transduction pathway. Downregulation of Bcl-2 and the overexpression of Bax by QUE-NL supported the involvement of Bcl-2 family proteins upstream of C6 glioma cell death. In addition, the activation of JAK2 and STAT3 were altered following exposure to QUE-NLs in C6 glioma cells, suggesting that QUE-NLs downregulated Bcl-2 mRNAs expression and enhanced the expression of mitochondrial mRNAs through STAT3-mediated signaling pathways either via direct or indirect mechanisms. There are several components such as ROS, mitochondrial, and Bcl-2 family shared by the necrotic and apoptotic pathways. Our studies indicate that the signaling cross point of the mitochondrial pathway and the JAK2/STAT3 signaling pathway in C6 glioma cell death is modulated by QUE-NLs. In conclusion, regulation of JAK2/STAT3 and ROS-mediated mitochondrial pathway agonists alone or in combination with treatment by QUE-NLs could be a more effective method of treating chemical-resistant glioma.https://doi.org/10.1038/cddis.2013.242quercetin nanoliposomesprogrammed cell deathJAK2/STAT3mitochondrial pathway |
| spellingShingle | G Wang J J Wang X L Chen S M Du D S Li Z J Pei H Lan L B Wu RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell death Cell Death and Disease quercetin nanoliposomes programmed cell death JAK2/STAT3 mitochondrial pathway |
| title | RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell death |
| title_full | RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell death |
| title_fullStr | RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell death |
| title_full_unstemmed | RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell death |
| title_short | RETRACTED ARTICLE: The JAK2/STAT3 and mitochondrial pathways are essential for quercetin nanoliposome-induced C6 glioma cell death |
| title_sort | retracted article the jak2 stat3 and mitochondrial pathways are essential for quercetin nanoliposome induced c6 glioma cell death |
| topic | quercetin nanoliposomes programmed cell death JAK2/STAT3 mitochondrial pathway |
| url | https://doi.org/10.1038/cddis.2013.242 |
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