中国医科大学学报

中国医科大学学报
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中国医科大学学报 ›› 2018, Vol. 47 ›› Issue (5): 394-397.doi: 10.12007/j.issn.0258-4646.2018.05.003

• 论著 • 上一篇    下一篇

瞬时感受器电位香草酸受体3促进胶质瘤U251细胞系增殖和侵袭

李忠华1, 李慧峰2, 李晓蕾3   

  1. 1. 贵州医科大学第三附属医院神经外科, 贵州 都匀 558000;
    2. 大庆油田总医院病理科, 黑龙江 大庆 163001;
    3. 贵州医科大学第三附属医院实验中心, 贵州 都匀 558000
  • 收稿日期:2018-03-14 出版日期:2018-05-30 发布日期:2018-04-27
  • 通讯作者: 李晓蕾 E-mail:xiaoleili2004@163.com
  • 作者简介:李忠华(1978-),男,副主任医师,博士.
  • 基金资助:
    国家自然科学基金(81660386);贵州省科技合作计划(20157372);贵州省卫计委科学技术基金(gzwjkj2015-1-043)

Transient Receptor Potential Vanilloid 3 Promotes Proliferation and Invasion in Glioma U251 Cells

LI Zhonghua1, LI Huifeng2, LI Xiaolei3   

  1. 1. Department of Neurosurgery, The Third Affiliated Hospital of Guizhou Medical University, Duyun 558000, China;
    2. Department of Pathology, General Hospital of Daqing Oil Field, Daqing 163001, China;
    3. Department of Medical Experimental Center, The Third Affiliated Hospital of Guizhou Medical University, Duyun 558000, China
  • Received:2018-03-14 Online:2018-05-30 Published:2018-04-27

摘要: 目的 研究瞬时感受器电位香草酸受体3(TRPV3)通道蛋白对胶质瘤U251细胞系增殖和侵袭的影响及分子机制。方法 应用siRNA技术敲除U251细胞中TRPV3的表达,MTT方法检测细胞的增殖能力,Western blotting检测增殖细胞核抗原(PCNA)、基质金属蛋白酶(MMP)-2和MMP-9、钙/钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)和细胞周期蛋白D1(cyclin D1)的表达。结果 敲除TRPV3表达后U251细胞增殖和侵袭能力下降,磷酸化的CaMKⅡ和cyclin D1的表达也受到抑制。结论 TRPV3通道蛋白能够促进胶质瘤U251细胞的增殖和侵袭能力。其机制是TRPV3通道开放,细胞外Ca2+内流,cyclin D1过表达促进细胞的增殖。

关键词: 瞬时感受器电位香草酸受体3, 胶质瘤, 增殖, 侵袭, 细胞周期蛋白D1

Abstract: Objective To study the effect of transient receptor potential vanilloid 3(TRPV3)channel protein on the proliferation and invasion in glioma U251 cell line and its molecular mechanism.Methods TRPV3 expression was knocked down using siRNA technology in glioma U251 cells. The MTT method was used for detection of cell proliferation. Western blotting was performed to detect the expression of proliferating cell nuclear antigen(PCNA),matrix metalloproteinase(MMP)-2 and MMP-9,calcium/calmodulin-dependent kinase Ⅱ (CaMKⅡ),and cyclin D1.Results Knockdown of TRPV3 expression inhibited U251 cell proliferation and invasion and the expression of phosphorylated CaMKⅡand cyclin D1.Conclusion TRPV3 channel protein can promote the proliferation and invasion of glioma U251 cells. The mechanism is overexpression of cyclin D1 via extracellular Ca2+ influx,induced by the opening of the TRPV3 channel.

Key words: transient receptor potential vanilloid 3, glioma, proliferation, invasion, cyclin D1

中图分类号: 

  • R730.231
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