基础医学与临床 ›› 2019, Vol. 39 ›› Issue (10): 1460-1466.

• 研究论文 • 上一篇    下一篇

锌指蛋白12过表达促进甲状腺癌细胞的增殖并抑制其凋亡

刘光霞1,陈芳1,赵连春2,侯瞻1,高伟1,卢亚敏1   

  1. 1. 河北省人民医院
    2. 河北以岭医院
  • 收稿日期:2019-02-20 修回日期:2019-06-12 出版日期:2019-10-05 发布日期:2019-09-25
  • 通讯作者: 卢亚敏 E-mail:yamin_yml@163.com

ZCCHC12 overexpression promotes proliferation and inhibits apoptosis of thyroid cancer cell

  • Received:2019-02-20 Revised:2019-06-12 Online:2019-10-05 Published:2019-09-25

摘要: 目的 探讨smad-相互作用锌指蛋白12(ZCCHC12)对甲状腺癌细胞增殖和凋亡的影响及其机制。方法 采用Western blot检测30例甲状腺癌患者癌组织和癌旁组织中ZCCHC12的蛋白表达及细胞中cleaved caspase-3、caspase-9、BMP-2、p-smad1、smad 1和ID3的蛋白表达。ZCCHC12过表达质粒pcDNA3.1-ZCCHC12或抑制质粒ZCCHC12 siRNA转染甲状腺癌细胞系CGTH W-3和FTC-133。MTT法检测细胞增殖。流式细胞仪检测细胞凋亡。结果 ZCCHC12的表达在甲状腺癌组织较癌旁组织中显著增加(P<0.05)。ZCCHC12过表达显著增强了CGTH W-3和FTC-133的细胞增殖、降低了细胞凋亡、抑制了凋亡蛋白cleaved caspase-3和caspase-9的表达并升高了BMP-2、p-SMAD1和ID3的蛋白表达(P<0.05)。ZCCHC12抑制质粒则与过表达质粒作用相反。结论 ZCCHC12通过调控BMPs/smad通路增强甲状腺癌细胞CGTH W-3和FTC-133的增值并抑制其凋亡。

关键词: 甲状腺癌, CGTH W-3, FTC-133, ZCCHC12, BMPs/smad

Abstract: Objective To investigate the effect and underlying mechanism of zinc finger CCHC-type containing 12 (ZCCHC12) in regulating thyroid cancer cell proliferation and apoptosis. Methods The protein expression of ZCCHC12 in cancer tissues and non-tumor normal tissue in 30 thyroid cancer patients, and expression of cleaved caspase-3, caspase-9, BMP-2, p-smad1, smad 1, ID3 in thyroid cancer cells were measured by western blot. ZCCHC12 overexpression vector (pcDNA3.1-ZCCHC12) or inhibition vector (ZCCHC12 siRNA) was transfected into thyroid cancer cell line CGTH W-3 or FTC-133, respectively. Cell proliferation was measured by MTT method. Cell apoptosis was detected by flow cytometry. Results The protein expression of ZCCHC12 was significantly increased in thyroid cancer tissue compared with non-tumor normal tissue (P<0.05). ZCCHC12 overexpression significantly elevated cell proliferation, decreased cell apoptosis, inhibited expression of apoptosis-related protein cleaved caspase-3 and caspase-9, and increased protein expression of BMP-2, p- smad 1 and ID3 in CGTH W-3 and FTC-133 (P<0.05). The effect of ZCCHC12 inhibition vector was opposite from over-expression vector. Conclusions ZCCHC12 elevates the proliferation and inhibits the apoptosis of CGTH W-3 and FTC-133 cells through regulating BMPs/smad pathway.

Key words: Thyroid cancer, CGTH W-3, FTC-133, ZCCHC12, BMPs/smad