Suppression of Amp activated protein kinase activity enhance the radiosensitivity of human nasopharyngeal carcinoma cells
10.3969/j.issn.1671-8348.2014.22.025
- VernacularTitle:抑制磷酸腺苷激活的蛋白激酶活性增强人鼻咽癌细胞放射敏感性
- Author:
Xiaodi LU
;
Xiaodong ZHU
;
Wei ZHAO
;
Song QU
;
Xia LIANG
;
Fang SU
;
Hui MA
- Publication Type:Journal Article
- Keywords:
AM PK;
inhibitor;
nasopharyngeal carcinoma;
radiosensitivity;
autophagy
- From:
Chongqing Medicine
2014;(22):2900-2902
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of Amp activated protein kinase(AMPK)activity in radiosensitivity of human na-sopharyngeal carcinoma cells .Methods Human nasopharyngeal carcinoma cells ,CNE-2 ,were treated with AMPK inhibitor ,Com-pound C(CC) ,for 1 h .Then cells were explored in X-ray .The expression of total AMPK (t-AMPK) ,phosphorylation AMPK (p-AMPK) ,and MAPlLC3 were detected by Western blot .The number of autophagosomes were observed and calculated by transmis-sion electron microscope(TEM) .Cells processed with CC were explored in X-ray .MTT assay was used to detect the difference of two groups in cell proliferation .Cell apoptosis were assayed by flow cytometry .Results The expression of p-AMPK in CC group cells were significantly downregulated compared to the negative control group cells (P< 0 .01) ,while no significant change of t-AMPK expression were found(P>0 .05) .The expression of MAPlLC3 and the number of autophagosomes in CC group cells were significantly decreased compared to the control group cells (P<0 .05) .Correspondingly ,the cell proliferation rate in CC group was lower than in control group ,and the percent of apoptosis cells was higher in CC group than in control group (P<0 .05) .Conclusion Suppression of AM PK activity could inhibited autophagy induced by decreasing the degree of p-AM PK ,then enhanced the effect of proliferation inhibition and apoptosis promotion in CNE-2 cells .The AMPK inhibitor ,CC ,can serve as an effective assistant treatment of radiotherapy for nasopharyngeal carcinoma .
