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Quercetin Regulates Sestrin 2-AMPK-mTOR Signaling Pathway and Induces Apoptosis via Increased Intracellular ROS in HCT116 Colon Cancer Cells

BACKGROUND: The suppression of abnormal cell proliferation is therapeutic strategies for the treatment of cancer. In this study, we investigated the regulatory mechanism of quercetin-induced apoptosis through regulation of Sestrin 2 and AMPK signaling pathway. METHODS: After treatment of quercetin t...

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Detalles Bibliográficos
Autores principales: Kim, Guen Tae, Lee, Se Hee, Kim, Young Min
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society of Cancer Prevention 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4189461/
https://www.ncbi.nlm.nih.gov/pubmed/25337554
http://dx.doi.org/10.15430/JCP.2013.18.3.264
Descripción
Sumario:BACKGROUND: The suppression of abnormal cell proliferation is therapeutic strategies for the treatment of cancer. In this study, we investigated the regulatory mechanism of quercetin-induced apoptosis through regulation of Sestrin 2 and AMPK signaling pathway. METHODS: After treatment of quercetin to colon cancer cells, intracellular ROS was detected using by DCFH-DA. To examine how quercetin and H(2)O(2) induced apoptosis, we analyzed the change of Sestrin 2, p53 expression and p-AMPKα1, p-mTOR levels by Western blotting. To evaluate the effect of intracellular ROS generated by quercetin on colon cancer cells, NAC, anti-oxidative agent, was co-treated. RESULTS: Quercetin increased apoptotic cell death though generating intracellular reactive oxygen species (ROS), and it was responsible for Sestrin 2 expression. Increased Sestrin 2 expression was accompanied by AMPK activation. Interestingly, mTOR activity by Sestirn 2 expression was dependent on AMPK phosphorylation. On the other hand, the expression of Sestrin 2 by quercetin-generated intracellular ROS was independent of p53. CONCLUSIONS: We suggested that quercetin-induced apoptosis involved Sestrin 2/AMPK/mTOR pathway, which was regulated by increased intracellular ROS by quercetin.