Kazinol C from Broussonetia kazinoki activates AMP-activated protein kinase to induce antitumorigenic effects in HT-29 colon cancer cells
- Authors
- Kim, Hak-Su; Lim, Jihyun; Lee, Da Yeon; Ryu, Jae-Ha; Lim, Jong-Seok
- Issue Date
- Jan-2015
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- kazinol C; AMP-activated protein kinase; apoptosis; migration; colon cancer
- Citation
- ONCOLOGY REPORTS, v.33, no.1, pp 223 - 229
- Pages
- 7
- Journal Title
- ONCOLOGY REPORTS
- Volume
- 33
- Number
- 1
- Start Page
- 223
- End Page
- 229
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10704
- DOI
- 10.3892/or.2014.3601
- ISSN
- 1021-335X
1791-2431
- Abstract
- Kazinol C is a 1,3-diphenylpropane, obtained from Broussonetia kazinoki, that has been employed in folk medicine as an edema suppressant. It exerts beneficial effects in oxidative stress-related diseases, such as cancer. However, the molecular mechanism involved in the anticancer effects remains to be determined. AMP-activated protein kinase (AMPK) has emerged as a possible anticancer target molecule. The present study investigated the effect of kazinol C on AMPK activation as well as subsequent HT-29 colon cancer cell viability, apoptosis and migration. Kazinol C markedly induced AMPK phosphorylation and significantly attenuated HT-29 colon cancer cell growth and viability. Compound C, as a well-known AMPK inhibitor, blocked the kazinol C-induced cell death, and stable transduction of dominant-negative (DN) AMPK in colon cancer cells also inhibited kazinol C-induced cell apoptosis. In addition, kazinol C inhibited HT-29 cell migration and anchorage-independent growth. AMPK inhibition using stable transduction with DN AMPK significantly abrogated the kazinol C-induced inhibition of cancer cell migration. Thus, AMPK is a critical and novel regulator of kazinol C-mediated cancer cell apoptosis and inhibition of migration, suggesting that AMPK is a prime cancer target.
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