TITLE

绿原酸对体外培养的人鼻咽癌细胞株CNE-1的作用

AUTHOR(S)
姚素艳; 李全胜; 郑德宇
PUB. DATE
November 2014
SOURCE
Journal of Xi'an Jiaotong University (Medical Sciences);Nov2014, Vol. 35 Issue 6, p838
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Objective To explore the effects and mechanisms of chlorogenic acid (CHA) on the human nasopharyngeal carcinoma cell line CNE-1 cultured in vitro. Methods The human nasopharyngeal carcinoma cell line CNE-1 underwent resuscitation in sterile conditions. CHA was added into the CNE-1 culture media at the concentrations of 0, 25, 50, 100, 200 and 500μmol/L for 7 days. The optimal concentration of CHA which inhibited the CNE-1 was determined by CCK8 inhibition experiment in vitro. After CNE-1 was cultured at the optimal concentration of CHA for 10 days, telomerase activation was detected by ELISA method. The expressions of anti-oncogene p27 and p16 as well as cyclin D1 and CDK4 were determined by Western blot. Results The optimal concentration of CHA for inhibiting CNE-1 cell line was 100μmol/L determined by CCK8 inhibition experiment. Telomerase activation of CNE-1 was decreased to 1.621 after CNE-1 was treated with 100μmol/L CHA for 10 days. The activation was significantly lower than that in the positive group and the normal cultured CNE-1 group (P<0.01). Anti-oncogene p27 and p16 were expressed in a low quantity after CNE-1 was treated with 100μmol/L CHA for 10 days. But there was hardly any p27 or p16 expression in the positive group (HT1080) and the normal cultured CNE-1 group (CHA concentration being 0μmol/L) determined by Western blot method. The expressions of cyclin D1 and cyclin dependence kinase 4 (CDK4) were lower after CNE-1 received 100μmol/L CHA for 10 days than those in the HT1080 cell line and the normal cultured CNE-1 (CHA concentration being 0μmol/L). Conclusion CHA has the functions of decreasing telomerase activation of CNE-1 cell line, increasing the anti-oncogene expression and decreasing cyclin D1 expression. The inhibitory function of CHA on CNE-1 cell line is realized by activating the expression of anti-oncogene and inhibiting the expression of cyclin D1.
ACCESSION #
99643696

 

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