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.