›› 2015, Vol. 6 ›› Issue (4): 178-182.

• 论著 • 上一篇    下一篇

let-7i影响口腔鳞癌增殖和迁移作用的研究

赵珍1,李新明2,张建军1,秦星1,孙强2,陈万涛3   

  1. 1. 上海交通大学医学院附属第九人民医院口腔颌面-头颈肿瘤科
    2. 郑州大学第一附属医院口腔颌面外科
    3. 上海交通大学医学院附属第九人民医院
  • 收稿日期:2015-09-08 修回日期:2015-11-24 出版日期:2015-12-25 发布日期:2015-12-30
  • 通讯作者: 陈万涛 E-mail:chenwantao2002@hotmail.com
  • 基金资助:
    国家自然科学基金重大研究计划(培育)项目;教育部博士点基金(导师)项目;上海市科学技术委员会项目

Study of let-7i effects on oral cancer proliferation and migration

  • Received:2015-09-08 Revised:2015-11-24 Online:2015-12-25 Published:2015-12-30

摘要: 目的:探讨微小RNA let-7i对口腔鳞癌细胞的增殖、凋亡、侵袭及迁移调控的作用。方法:荧光定量PCR(qRT-PCR)检测口腔鳞癌组织与癌旁正常组织之间let-7i的表达差异,并在口腔鳞癌细胞系和正常口腔上皮细胞系中进行表达水平验证。应用let-7i抑制物和模拟物转染口腔鳞癌细胞系(SCC25)细胞,qRT-PCR检测let-7i的抑制或者增强效率;应用细胞增殖实验、单细胞克隆形成实验、细胞凋亡实验、Transwell细胞迁移和侵袭实验等技术,分别检测let-7i表达水平变化对口腔鳞癌细胞生长、迁移和侵袭等生物学行为的影响。结果:与癌旁正常组织相比,口腔鳞癌组织中let-7i的表达显著上调,为癌旁正常组织表达量的1.97倍;let-7i抑制物和模拟物,能分别显著降低或增强SCC25中let-7i的表达;降低let-7i表达后,SCC25细胞的增殖能力、迁移和侵袭能力明显降低;而细胞凋亡率明显升高;相反let-7i表达升高后,SCC25细胞增殖能力、Transwell迁移和侵袭能力明显升高,而凋亡率明显降低。结论:let-7i能够促进口腔鳞癌细胞的增殖、迁移和侵袭,而其抑制物能发挥有效的抗增殖作用,为口腔鳞癌的靶向治疗提供了候选分子。

Abstract: Objective:To investigate the regulation of let-7i on the cell proliferation, apoptosis, migration and invasion in oral squamous cell carcinoma (OSCC). Methods:The expressions of let-7i were measured in OSCC tissues, the adjacent normal tissues and OSCC cell lines by qRT-PCR to investigate the differentiation of paired samples. The inhibition or enhancement of let-7i in OSCC cells after let-7i inhibitor or let-7i mimics were transfected into the cells. Then cell proliferation, single cell clone formation, flow cytometry, transwell migration and invasion tests were carried out to study the effects of let-7i on biological behaviors of OSCC cells. Results:The expression of let-7i increased in OSCC tissues(n=29, t=8.215, P<0.01)and cell lines compared with adjacent normal tissues. Let-7i inhibitor or mimics could decrease or enhance the expressions of let-7i in SCC25 cells significantly. After let-7i inhibitor was transfected, the cell proliferation, cell migration and invasion abilities of SCC25 cells were reduced significantly, and higher apoptotic rate was observed. Instead, when transfected with let-7i mimics, SCC25 cells showed an opposite change on biological behaviors. Conclusions:Let-7i can promote the cell proliferation, migration and invasion in OSCCs. As let-7i inhibitor is an effective anticancer factor by interfering with let-7i, providing us a novel candidate to treat OSCCs.