Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0613820140240010092
Journal of Life Science
2014 Volume.24 No. 1 p.92 ~ p.97
Induction of Apoptosis and G2/M Cell Cycle Arrest by Cordycepin in Human Prostate Carcinoma LNCap Cells
Lee Hye-Hyeon

Hwang Won-Deok
Jeong Jin-Woo
Park Cheol
Han Min-Ho
Hong Su-Hyun
Jeong Yong-Kee
Choi Yung-Hyun
Abstract
Cordycepin, an active component originally isolated from the traditional medicine Cordyceps militaris, is a derivative of the nucleoside adenosine, which has been shown to possess a number of pharmacological properties, including antioxidant and anti-inflammatory activities, immunological stimulation, and antitumor effects. This study was conducted on cultured human prostate carcinoma LNCap cells to elucidate the possible mechanisms by which cordycepin exerts its anticancer activity, which, until now, has remained poorly understood. Cordycepin treatment of LNCap cells resulted in dose-dependent inhibition of cell growth and the induction of apoptotic cell death as detected by an MTT assay, cleavage of poly ADP-ribose polymerase, and annexin V-FITC staining. Flow cytometric analysis revealed that cordycepin resulted in G2/M arrest in cell cycle progression and downregulation of cyclin B1 and cyclin A expression in a concentration-dependent manner. Moreover, the incubation of cells with cordycepin caused a striking induction in the expression of the cyclin-dependent kinase (CDK) inhibitor p21Waf1/Cip1 without affecting the expression of the tumor suppressor p53. It also resulted in a significant increase in the binding of CDK2 and CDC2 to p21. These findings suggest that cordycepin-induced G2/M arrest and apoptosis in human prostate carcinoma cells is mediated through p53-independent upregulation of the CDK inhibitor p21.
KEYWORD
Apoptosis, cordycepin, G2/M arrest, p21, prostate carcinoma LNCap cells
FullTexts / Linksout information
Listed journal information
ÇмúÁøÈïÀç´Ü(KCI)