|本期目录/Table of Contents|

[1]段 娟,徐 燕,廖之君,等.核糖体小亚基蛋白S7对结肠癌细胞HCT116迁移的作用初探[J].福建医科大学学报,2016,50(05):281-284.
 DUAN Juan,XU Yan,LIAO Zhijun,et al.The Discussion of the Effect of Ribosomal Protein S7 on theMigration of Human Colon Cancer Cells HCT116[J].Journal of Fujian Medical University,2016,50(05):281-284.
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《福建医科大学学报》[ISSN:1672-4194/CN:35-1192/R]

卷:
第50卷
期数:
2016年05期
页码:
281-284
栏目:
论著
出版日期:
2016-10-31

文章信息/Info

Title:
The Discussion of the Effect of Ribosomal Protein S7 on theMigration of Human Colon Cancer Cells HCT116
文章编号:
1672-4194(2016)05-0281-04
作者:
段 娟 徐 燕 廖之君 郑志竑 何 艳
福建医科大学 基础医学院生物化学与分子生物学系,福州 350108
Author(s):
DUAN Juan XU Yan LIAO Zhijun ZHENG Zhihong HE Yan
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences,Fujian Medical University, Fuzhou 350108, China
关键词:
核糖体蛋白质类/*生物合成 RNA小分子干扰 基因p53 细胞运动 结肠肿瘤 HCT116细胞
Keywords:
ribosomal proteins/* biosynthesis RNA small interfering genes p53 cell movement colonic neoplasms HCT116 cells
分类号:
R329.24; R329.25
DOI:
-
文献标志码:
A
摘要:
目的 探讨核糖体小亚基蛋白S7(RPS7)对结肠癌细胞HCT116迁移的作用及机制。 方法 以3种基因型人结肠癌HCT116细胞株(p53野生型,p53-/-,p21-/-)为研究对象,利用pCDNA3.1-s7质粒对rps7基因进行过表达,rps7小分子干扰RNA对rps7基因进行沉默,实时定量PCR检测转染前后细胞rps7 mRNA的表达变化,Transwell细胞迁移实验观察细胞迁移能力的改变。 结果 3种不同的HCT116细胞株转染了pCDNA3.1-s7质粒后,rps7基因的表达均明显上调,且迁移能力均受到显著促进,增幅大小依次为HCT116(p53-/-)>HCT116(WT)>HCT116(p21-/-); 而转染了rps7 siRNA后,rps7基因的表达均明显下调,且迁移能力均受到显著抑制,减幅大小依次为HCT116(p53-/-)>HCT116(p21-/-)>HCT116(WT)。 结论 RPS7对结肠癌细胞HCT116迁移运动的促进作用显著,且该作用与细胞内的P53水平有关,提示RPS7可能通过P53通路或者其他机制在结肠癌细胞HCT116的迁移中发挥重要作用。
Abstract:
Objective To study the effect and mechanism of rps7 on the migration of human colon cancer cells HCT116 in vitro. Methods The three kinds of human colon cancer cells HCT116(p53 WT,p53-/-,p21-/-)were transfected by pCDNA3.1-s7 plasmid to overexpression rps7 gene or rps7 siRNA to silence rps7 gene. The mRNA level of rps7, before and after transfection, was examined by real-time quantitative RT-PCR(QPCR)respectively. Then the migration capability was evaluated by tumor migration assay. Results In three different HCT116 cells, the transfection of pCDNA3.1-s7 plasmid could specifically up-regulate the rps7 mRNA, and the upregulation of rps7 promoted the migration capability with the increased range in the order of HCT116(p53-/-)> HCT116(WT)> HCT116(p21-/-). The transfection of rps7 siRNA could down-regulate the rps7 mRNA, and this downregulation suppressed the migration capability, and the decrease range is HCT116(p53-/-)> HCT116(p21-/-)>HCT116(WT). Conclusion rps7 obviously promoted the migration of HCT116 cells in vitro,and the influence was related with P53 level in cells. These results suggest that RPS7 may play an important role in the malignant progression in colon cancer cells HCT116, through P53 pathway or other unknown mechanism.

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备注/Memo

备注/Memo:
收稿日期: 2016-03-18
基金项目: 福建省自然科学基金青年基金(2013J05048); 福建医科大学博士启动基金(2011BS001)
作者单位: 福建医科大学 基础医学院生物化学与分子生物学系,福州 350108
作者简介: 段 娟(1982-),女,讲师,理学博士
通讯作者: 何 艳. Email: hyhyj2002@163.com
更新日期/Last Update: 2016-10-31