二甲双胍诱导甲状腺乳头状癌BCPAP细胞的凋亡

董丽儒; 李敏; 李双; 刘爱东; 熊艳杰; 唐慧; 宋旭东

doi:10.13201/j.issn.1001-1781.2017.12.010

二甲双胍诱导甲状腺乳头状癌BCPAP细胞的凋亡

- 1 华北理工大学附属医院病理科(河北唐山, 063000);
- 2 华北理工大学附属医院药剂科
基金项目:
河北省卫计委医学重点课题 (No:20170928)

详细信息

通讯作者: 宋旭东,E-mail:songxd2002@sina.com

中图分类号: R736.1

收稿日期: 2017-01-22

Metformin induced apoptosis of papillary thyroid carcinoma BCPAP cells

- 1 Department of Pathology, Affiliated Hospital of North China University of Science and Technology, Tangshan, 063000, China;
- 2 Department of Pharmacy, Affiliated Hospital of North China University of Science and Technology

More Information

Corresponding author: SONG Xudong, E-mail: songxd2002@sina.com

Received Date: 22 January 2017

摘要

摘要: 目的:探讨二甲双胍对甲状腺乳头状癌BCPAP细胞凋亡的影响及其机制。方法:MTT实验分别检测不同浓度(0 mmol/L,1 mmol/L,5 mmol/L,10 mmol/L,20 mmol/L)二甲双胍和20 mmol/L二甲双胍不同时间点(0 h,4 h,8 h,16 h,24 h,48 h)对PTC细胞系BCPAP细胞增殖的影响。流式细胞术检测二甲双胍对细胞凋亡的影响,Western blot检测GRP78、CHOP、Caspase-12蛋白的表达。结果:与0 mmol/L对照组相比,1 mmol/L至20 mmol/L的二甲双胍可有效降低BCPAP癌细胞的增殖活性(P<0.05);20 mmol/L二甲双胍处理BCPAP癌细胞48 h后,可呈现明显细胞凋亡,且内质网应激相关蛋白GRP78、CHOP和Caspase-12表达明显增加(P<0.05)。而抑制剂组则可降低BCPAP癌细胞的凋亡率和内质网应激相关蛋白GRP78、CHOP和Caspase-12的表达(P<0.05)。结论:二甲双胍可以通过启动内质网应激有效参与诱导BCPAP细胞凋亡。
- 甲状腺乳头状癌 /
- 二甲双胍 /
- 内质网应激 /
- 凋亡
Abstract: Objective: To investigate the role of metformin in inducing apoptosis of papillary thyroid carcinoma BCPAP cells.Method: Using MTT methods to detect effects of metformin on cell proliferation of BCPAP in different concentrations(0 mmol/L, 1 mmol/L, 5 mmol/L, 10 mmol/L, 20 mmol/L)and time course(0 h, 4 h, 8 h, 16 h, 24 h, 48 h). The experiment was divided into four groups: Con, Met, Met+Sal and Met+DM, flow cytometry to detect the rate of apoptosis of BCPAP. Then detect the protein expressions of CHOP, GRP78 and Caspase-12 of 4 groups by Western blot.Result: Compared with the experimental control group, the percentage of cell proliferation index significantly decreased in metformin (0-20 mmol/L and 0-48 h) treatment group. Compared with the experimental control group, the percentage of apoptosis cells significantly increased in metformin treatment group. Compared with the control group, the protein expressions of GRP78,CHOP and Caspase-12 were significantly increased in Met group; While compared with the Met group, the protein expressions of GRP78,CHOP and Caspase-12 were significantly inhibited in the Met+Sal group.Conclusion: Metformin can induced availably BCPAP cell apoptosis by activating endoplasmic reticulum stress mechanism.
- papillary thyroid carcinoma /
- metformin /
- endoplasmic reticulum stress /
- apoptosis

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