| 王彦玲,吴慧,卢晓旭,等.多西紫杉醇对甲状腺乳头状癌细胞系的放射增敏研究[J].中华放射医学与防护杂志,2016,36(2):100-104.Wang Yanling,Wu Hui,Lu Xiaoxu,et al.Study of radiosensitization of docetaxel on papillary thyroid carcinoma cell lines[J].Chin J Radiol Med Prot,2016,36(2):100-104 |
| 多西紫杉醇对甲状腺乳头状癌细胞系的放射增敏研究 |
| Study of radiosensitization of docetaxel on papillary thyroid carcinoma cell lines |
| 投稿时间：2015-07-03 |
| DOI：10.3760/cma.j.issn.0254-5098.2016.02.004 |
| 中文关键词: 多西紫杉醇 甲状腺乳头状癌 放射敏感性 |
| 英文关键词:Docetaxel Papillary thyroid carcinoma Radiosensitivity |
| 基金项目:河南省医学科技攻关计划重点项目(201402034) |
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| 中文摘要: |
| 目的 研究多西紫杉醇对甲状腺乳头状癌TPC-1细胞系放射敏感性的影响。方法 6 MV X射线照射及多西紫杉醇单独或联合作用于细胞。采用CCK-8检测多西紫杉醇对TPC-1细胞增殖的影响;克隆形成法观察多西紫杉醇对TPC-1细胞放射敏感性的影响;流式细胞仪测定多西紫杉醇TPC-1细胞凋亡的变化和细胞周期的影响。Western blot法检测Bax、Bcl-2蛋白表达水平。结果 多西紫杉醇对TPC-1细胞系的增殖具有抑制作用,且存在明显的剂量和时间依赖性,半数抑制浓度分别为6.06(24 h)、1.39(48 h)和0.09μg/ml (72 h)。多西紫杉醇联合照射的SF2、D0、Dq较单纯照射均有所下降,放射增敏比(SER)为1.53。0.05μg/ml多西紫杉醇联合照射作用于TPC-1细胞24、48、72 h后凋亡率分别为31.67%、44.57%、70.20%,与单纯照射比较,差异具有统计学意义(t=-146.56、-15.13、-19.15,P<0.05)。多西紫杉醇使TPC-1细胞发生G2/M期阻滞。与单纯照射相比,紫杉醇联合照射能显著增加G2/M期细胞阻滞(t=-79.17,P<0.05),伴有Bax蛋白表达增加(t=93.56,P<0.05)和Bcl-2表达降低(t=41.02,P<0.05)。结论 多西紫杉醇能增加甲状腺乳头状癌TPC-1细胞的凋亡,使细胞周期再分布,可能是通过调节Bax、Bcl-2等相关蛋白表达增加其放射敏感性。 |
| 英文摘要: |
| 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. |
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