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Anticancer effect of icaritin inhibits cell growth of colon cancer through reactive oxygen species, Bcl-2 and cyclin D1/E signaling
Author(s) -
Chaofeng Li,
Weichao Peng,
Xin Song,
Qian Wang,
Wenyue Wang
Publication year - 2016
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.5089
Subject(s) - cyclin d1 , cell cycle , cancer research , apoptosis , cyclin , reactive oxygen species , cyclin d , cyclin b , cell growth , cancer , cancer cell , cyclin b1 , colorectal cancer , chemistry , cyclin e , biology , microbiology and biotechnology , biochemistry , cyclin dependent kinase 1 , genetics
Icaritin has an advantage in enhancing immunity. Besides, with its anticancer effect, it may be of great help in cancer treatment and recovery of cancer patients. As a result, icaritin is likely to become a novel anticancer drug. However, the anticancer effect of icaritin against colon cancer has not been elucidated thus far. The present study investigated the latent anticancer effect of icaritin on the inhibition of colon cancer cell growth by regulating reactive oxygen species (ROS), B-cell lymphoma (Bcl)-2 and cyclin D1/E signaling. The COLO-205 colon cancer cell line was used as a colon cancer cell model in the present study. First, cell growth and apoptosis were measured to analyze the anticancer effect of icaritin against colon cancer. Next, the possible mechanism of icaritin against colon cancer, including ROS, Bcl-2, cyclin D1, cyclin E and caspase-3/9, was explored. The results revealed that icaritin could inhibit cell growth and induce the apoptosis of COLO-205 cells. In addition, icaritin significantly induced ROS generation, suppressed Bcl-2, cyclin D1 and cyclin E protein expression, and activated caspase-3/9 activity in COLO-205 cells. The present findings demonstrated that icaritin exerted antiproliferative and anticancer effects against colon cancer through the activation of ROS generation and the suppression of Bcl-2, cyclin D1 and cyclin E signaling.

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