Study of radiosensitization of docetaxel on papillary thyroid carcinoma cell lines
10.3760/cma.j.issn.0254-5098.2016.02.004
- VernacularTitle:多西紫杉醇对甲状腺乳头状癌细胞系的放射增敏研究
- Author:
Yanling WANG
;
Hui WU
;
Xiaoxu LU
;
Xueming SUN
;
Jing XU
;
Rong HUANG
- Publication Type:Journal Article
- Keywords:
Docetaxel;
Papillary thyroid carcinoma;
Radiosensitivity
- From:
Chinese Journal of Radiological Medicine and Protection
2016;36(2):100-104
- CountryChina
- Language:Chinese
-
Abstract:
Objective To research the influence of docetaxel on radiosensitivity in papillary thyroid carcinoma TPC-1 cells.Methods 6 MV X-ray irradiation and deocetaxel were incubated separately or jointly with TPC-1 cells.Proliferation inhibition of docetaxel on TPC-1 cells was detected by CCK-8 method.Radiosensitization of docetaxel was measured by clone formation assay.Flow cytometry (FCM) was employed to analyze cell apoptosis and cycle progression.Western blot assay was applied to examine the expressions of Bax and Bcl-2 proteins.Results The proliferation inhibition effect depended on the concentration and treatment time of docetaxel with IC50 value of 6.06 (24 h),1.39 (48 h),and 0.09 μg/ml (72 h),respectively.The value of SF2,D0,Dq in the radiation treatment group combined with docetaxel were obviously lower than those in the radiation alone group.The SER of docetaxel was 1.53.Following treatment with 0.05 μg/ml docetaxel combined with radiation for 24,48,72 h,the ratios of apoptosis in TPC-1 cells were 31.67％,44.57％,70.20％,which were higher than that of radiation alone group(t =-146.56,-15.13,-19.15,P ＜ 0.05).FCM measurement showed that cell cycle arrest in G2/M phase in the cells treated with docetaxel and radiation was much more obvious than the group of radiation alone (t =-79.17,P ＜ 0.05).In addition,in the combination treatment group,the expression of Bax increased (t =93.56,P ＜ 0.05) while the expression of Bcl-2 decreased (t =41.02,P ＜ 0.05).Conclusions Docetaxel can enhance the radiosensitivity of TPC-1 cells by promoting cell cycle arrest,induction of apoptosis and formation of associated proteins Bax/Bcl-2.
