miR-26a suppresses gastric cancer cell invasion by targeting MMP16

陈治宇; 王辰辰; 胡　健

doi:10.19401/j.cnki.1007-3639.2016.10.002

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miR-26a suppresses gastric cancer cell invasion by targeting MMP16

更新时间：2025-12-31

- miR-26a suppresses gastric cancer cell invasion by targeting MMP16
- China Oncology Vol. 26, Issue 10, Pages: 813-819(2016)
- 作者机构：
  
  1. 复旦大学附属肿瘤医院肿瘤内科，复旦大学上海医学院肿瘤学系,上海,200032
  2. 中国人民解放军第四五五医院消化内科,上海,200052
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2016.10.002
  CLC：
- Published Online：17 November 2016，
  
  Published：17 November 2016
- 稿件说明：
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陈治宇,王辰辰,胡　健,等. miR-26a靶向MMP16参与调控胃癌细胞侵袭作用研究[J]. 中国癌症杂志, 2016, 26(10): 813-819.

陈治宇, 王辰辰, 胡　健. miR-26a suppresses gastric cancer cell invasion by targeting MMP16[J]. China Oncology, 2016, 26(10): 813-819.
陈治宇,王辰辰,胡　健,等. miR-26a靶向MMP16参与调控胃癌细胞侵袭作用研究[J]. 中国癌症杂志, 2016, 26(10): 813-819. DOI： 10.19401/j.cnki.1007-3639.2016.10.002.

陈治宇, 王辰辰, 胡　健. miR-26a suppresses gastric cancer cell invasion by targeting MMP16[J]. China Oncology, 2016, 26(10): 813-819. DOI： 10.19401/j.cnki.1007-3639.2016.10.002.

摘要

背景与目的：胃癌发生侵袭转移是导致患者预后不良的重要因素。本研究旨在明确miR-26a在调控胃癌细胞运动侵袭中的作用及其可能机制。方法：通过实时荧光定量聚合酶链反应(real-time fluorescent quantitative polymerase chain reaction，RTFQ-PCR)检测胃癌组织细胞中miR-26a表达情况，体外通过CCK-8法、平板克隆形成实验和Matrigel-Transwell实验评价miR-26a对人胃癌细胞增殖、运动和侵袭能力的影响。荧光素酶报告基因系统评估miR-26a对下游靶基因的调控作用。结果：胃癌组织中miR-26a表达较癌旁组织明显下降。miR-26a体外对胃癌细胞增殖无明显影响，但可显著抑制胃癌细胞的运动和侵袭。相反，抑制miR-26a表达可促进胃癌细胞的侵袭能力。生物信息学分析提示，基质金属蛋白酶16(matrix metalloproteinase 16，MMP16)为miR-26直接调控靶基因，miR-26a可抑制胃癌细胞MMP16 miRNA和蛋白的表达。荧光素酶报告基因检测提示，miR-26a可与MMP16 mRNA 3’UTR结合诱导其转录后抑制。进一步研究提示，MMP16 siRNA对胃癌细胞侵袭具有模拟miR-26a作用，而过表达MMP16可拮抗miR-26a对胃癌细胞侵袭的影响。结论：miR-26a可通过靶向MMP16来抑制胃癌细胞运动侵袭，miR-26a可作为抑制胃癌细胞侵袭的重要干预靶点。

Abstract

Background and purpose: Invasion and metastasis lead to poor prognosis in gastric cancer. In this study

we investigated the potential function of miR-26a in gastric cancer. Methods: Real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the expression of miR-26a in gastric cancer cells. In vitro CCK-8 assay

cloning formation assay and Matrigel-Transwell assay were used to evaluate the proliferation

migration and invasion of gastric cancer cells. A luciferase reporter assay was also conducted to confirm that matrix metalloproteinase-16 (MMP16) is a direct target of miR-26a. Results: miR-26a was down-regulated in gastric cancer tissues compared with that in non-cancerous tissues. Functional studies showed that miR-26a inhibited cell proliferation

colony formation

cell motility and invasion. However

miR-26a had no effect on cell proliferation. We also characterized MMP16 as a direct target of miR-26a. We showed that knocking down MMP16 in gastric cancer cells significantly decreased MMP16 expression and inhibited cell invasion

whereas ectopic MMP16 expression significantly abrogated the suppressed cell invasion induced by miR-26a. Conclusion: miR-26a suppresses gastric cancer cell invasion by targeting MMP16. miR-26a could represent a potential therapeutic target for gastric cancer.

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