Journal
CHEMICO-BIOLOGICAL INTERACTIONS
Volume 300, Issue -, Pages 138-150Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2019.01.016
Keywords
Canolol; Apoptosis; ROS; Mitochondria; MAPK
Funding
- National Natural Science Foundation of China [31601438, 31471620, 31671820]
- Agricultural Science and Technology Innovation Project of Chinese Academy of Agricultural Sciences [CAAS-ASTIP-2013-OCRI]
- Earmarked Fund for China Agriculture Research System [CARS-13]
- National Key R&D Program of China [2016YFD0401401]
- Fundamental Research Funds for Central Non-profit Scientific Institution [1610172016003]
- Major Program of Technology Innovation Program of Hubei Province [2017ABA144]
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Canolol (4-vinylsyringol), extracted form crude canola oil, is the promising drug toward cancer prevention and treatment. The current studies focus on the role of COX-2 signaling pathway in canolol-induced apoptosis in cancer cells. It is still unknown whether mitochondria and MAPK signaling pathways are involved. To elucidate the roles of above signaling pathways in canolol-induced apoptosis in cancer cells, human cervical carcinoma cell line HeLa and HeLa xenograft tumor model are adopted. Canolol induced apoptosis of HeLa cells and inhibited tumor growth with low systemic adverse effect, accompanying with excess generation of intracellular ROS and lysosome rupture. The results in vitro and in vivo confirmed that MAPK signaling pathways mediated mitochondrial signaling pathway activation were involved in canolol-induced apoptosis. In conclusion, these data showed that canolol induced apoptosis in HeLa cells through ROS-MAPK mediated mitochondrial signaling pathway, providing a view of the potential application of canolol as an anticancer agent.
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