Article Search

Journal of Cancer Prevention

Original Article

Cancer prevention research 2011; 16(2): 118-125

Published online June 30, 2011

© Korean Society of Cancer Prevention

Modulation of Apoptosis in HepG2 Cells Via the Negative Regulation of mTOR and COX-2 with Curcumin

Song Yi Park1, Da Woon Jung1, Young Min Kim1 and Ock Jin Park2


Curcumin, a phytochemical claimed to be an effective cancer preventive effect, possibly through apoptosis. This study approached to address the mechanism for inducing apoptosis and the consequences of the treatment on the important signals of cancer cell control-mTOR (phospho-mammalian target of rapamycin) and COX-2 (cyclooxygenase-2). In curcumin-treated HepG2 hepatocarcinoma cells, the inhibition of cancer cell proliferation and the induction of apoptosis were observed. In order to explore the relationship between the decrement of p-mTOR and COX-2 expression induced by curcumin and the observed the inhibition of cell growth and the induction of apoptosis, the HepG2 cancer cells were treated with mTOR inhibitor rapamycin and COX-2 inhibitor, celecoxib respectively or in combination with curcumin. The greater decreased cell proliferation and the increased apoptosis were noticeable in the combination treatments of rapamycin and curcumin or celecoxib and curcumin. The depressed expressions of both mTOR and COX-2 were observed under the treatment of rapamycin alone or in combination of curcumin and rapamycin. However, the treatment of celecoxib alone was not resulted in the decreased mTOR expression even though the combined treatment of curcumin and celecoxib decreased COX-2 as well as mTOR. These results suggest that curcumin deareases cell proliferation and induces apoptosis by inhibiting p-mTOR and COX-2, and the inhibition of mTOR can modulate the expression of COX-2 but the inhibition of COX-2 may not influence mTOR. (Cancer Prev Res 16, 118-125, 2011)

Keywords: Curcumin, Apoptosis, HepG2 hepato-carcinoma cells, mTOR, COX-2

Share this article on :

Related articles in JCP

Most KeyWord