Journal
MOLECULAR MEDICINE REPORTS
Volume 13, Issue 3, Pages 2094-2100Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.4763
Keywords
myricetin; apoptosis; endoplasmic reticulum stress; DNA double-strand breaks; ovarian cancer
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Funding
- National Nature and Science foundation of China [NSFC81372793, 81272876]
- Department of Education of Jilin Province [2013361]
- Scientific Research Foundation of Jilin Province for University Students
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The mechanisms underlying myricetin-induced cancer cell apoptosis remain to be elucidated. Certain previous studies have shown that myricetin induces apoptosis through the mitochondrial pathway. Apoptosis, however, can also be induced by other classical pathways, including endoplasmic reticulum (ER) stress and DNA double-strand breaks (DSBs). The aim of the present study was to assess whether these two apoptotic pathways are involved in myricetin-induced cell death in SKOV3 ovarian cancer cells. The results revealed that treatment with myricetin inhibited viability of SKOV3 cells in a dose-dependent manner. Myricetin induced nuclear chromatin condensation and fragmentation, and also upregulated the protein levels of active caspase 3 in a time-dependent manner. In addition, myricetin upregulated ER stress-associated proteins, glucose-regulated protein-78 and C/EBP homologous protein in SKOV3 cells. Phosphorylation of H(2)AX, a marker of DNA DSBs, was revealed to be upregulated in myricetin-treated cells. The data indicated that myricetin induces DNA DSBs and ER stress, which leads to apoptosis in SKOV3 cells.
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