Wogonin induces apoptosis by activation of ERK and p38 MAPKs signaling pathways and generation of reactive oxygen species in human breast cancer cells
- Authors
- Yu, Ji Sun; Kim, An Keun
- Issue Date
- Apr-2011
- Publisher
- KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
- Keywords
- apoptosis; breast cancer; mitogen-activated protein kinases; reactive oxygen species; wogonin
- Citation
- MOLECULES AND CELLS, v.31, no.4, pp 327 - 335
- Pages
- 9
- Journal Title
- MOLECULES AND CELLS
- Volume
- 31
- Number
- 4
- Start Page
- 327
- End Page
- 335
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/12607
- DOI
- 10.1007/s10059-011-0041-7
- ISSN
- 1016-8478
0219-1032
- Abstract
- Wogonin is a one of the bioactive compounds of Scutellaria baicalensi Georgi which has been shown to have antiinflammatory, anticancer, antiviral and neuroprotective effects. However, the underlying mechanisms by which wogonin induces apoptosis in cancer cells still remain speculative. Here we investigated the potential activation of MAPKs and generation of reactive oxygen species (ROS) by wogonin on MCF-7 human breast cancer cells. These results showed that wogonin induced mitochondria and death-receptor-mediated apoptotic cell death, which was characterized by activation of several caspases, induction of PARP cleavage, change of antiapoptotic/proapoptotic Bcl-2 family member ratios and cleavage of Bid. We also found that generation of ROS was an important mediator in wogonin-induced apoptosis. Further investigation revealed that wogonin activated ERK and p38 MAPKs, which was inhibited by N-acetyl cysteine (NAC), a ROS scavenger, indicating that wogonin-induced ROS are associated with MAPKs activation. These data demonstrate that wogonin may be a novel anticancer agent for treatment of breast cancer.
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