miR-545 inhibited pancreatic ductal adenocarcinoma growth by targeting RIG-I

被引:49
|
作者
Song, Bin [1 ]
Ji, Weiping [1 ]
Gu, Shiwei [1 ]
Liu, Anan [1 ]
Jing, Wei [1 ]
Shao, Chenghao [1 ]
Li, Gang [1 ]
Jin, Gang [1 ]
机构
[1] Second Mil Med Univ, Dept Pancreat Surg, Changhai Hosp, Shanghai 200082, Peoples R China
基金
上海市自然科学基金;
关键词
miR-545; Pancreatic ductal adenocarcinoma; RIG-I; Patients survival; Cancer growth; HEPATOCELLULAR-CARCINOMA; MICRORNAS; CANCER; RECOGNITION; SURVIVAL; RNA; ACTIVATION; APOPTOSIS; GENES; CELLS;
D O I
10.1016/j.febslet.2014.10.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pancreatic ductal adenocarcinoma (PDAC) ranks fourth on the list of cancer-related causes of death. Deregulation or dysfunction of miRNAs contribute to cancer development. In this study, we found that low miR-545 level and high RIG-I protein in PDAC tissues were both correlated with low survival rate. MiR-545 up-regulation inhibited PDAC cell lines growth and vice versa. 3'UTR of RIG-I was targeted by miR-545. Thus we concluded that low miR-545 levels in PDAC promote tumor cells growth, and this is associated with reduced survival in PDAC patients. MiR-545 exerts its effects by directly targeting RIG-1. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:4375 / 4381
页数:7
相关论文
共 50 条
  • [11] miR-26a suppresses the growth and metastasis via targeting matrix metalloproteinase 14 in pancreatic ductal adenocarcinoma
    Zhong, Yuchuan
    Yao, Guowang
    Zhao, Guang
    Zhang, Dapeng
    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY, 2016, 9 (04): : 4803 - 4809
  • [12] RNF122 suppresses antiviral type I interferon production by targeting RIG-I CARDs to mediate RIG-I degradation
    Wang, Wendie
    Jiang, Minghong
    Liu, Shuo
    Zhang, Shikun
    Liu, Wei
    Ma, Yuanwu
    Zhang, Lianfeng
    Zhang, Jiyan
    Cao, Xuetao
    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2016, 113 (34) : 9581 - 9586
  • [13] Interplay of miR-21 and FoxO1 modulates growth of pancreatic ductal adenocarcinoma
    Song, Weifeng
    Wang, Lei
    Wang, Liwei
    Li, Qi
    TUMOR BIOLOGY, 2015, 36 (06) : 4741 - 4745
  • [14] MiR-202-5p Inhibits RIG-I-Dependent Innate Immune Responses to RGNNV Infection by Targeting TRIM25 to Mediate RIG-I Ubiquitination
    Liu, Wei
    Jin, Yilin
    Zhang, Wanwan
    Xiang, Yangxi
    Jia, Peng
    Yi, Meisheng
    Jia, Kuntong
    VIRUSES-BASEL, 2020, 12 (03):
  • [15] MiR-708-5p inhibits the progression of pancreatic ductal adenocarcinoma by targeting Sirt3
    Huang, Shanshan
    Guo, Hui
    Cao, Yuan
    Xiong, Jianping
    PATHOLOGY RESEARCH AND PRACTICE, 2019, 215 (04) : 794 - 800
  • [16] Downregulation of miR-124 predicts poor prognosis in pancreatic ductal adenocarcinoma patients
    Sun, BoLin
    Liu, Xiaogang
    Gao, Yewu
    Li, Li
    Dong, ZhenLing
    BRITISH JOURNAL OF BIOMEDICAL SCIENCE, 2016, 73 (04) : 152 - 157
  • [17] Expression of epidermal growth factors and apoptosis markers in pancreatic ductal adenocarcinoma
    Pryczynicz, Anna
    Guzinska-Ustymowicz, Katarzyna
    Czyzewska, Jolanta
    Kemona, Andrzej
    FOLIA HISTOCHEMICA ET CYTOBIOLOGICA, 2009, 47 (04) : 667 - 671
  • [18] Modulation of FoxO1 Expression by miR-21 to Promote Growth of Pancreatic Ductal Adenocarcinoma
    Song, Weifeng
    Li, Qi
    Wang, Lei
    Wang, Liwei
    CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2015, 35 (01) : 184 - 190
  • [19] The role of miR-10b in metastatic pancreatic ductal adenocarcinoma
    Frampton, Adam E.
    Krell, Jonathan
    Zhang, Yaojun
    Stebbing, Justin
    Castellano, Leandro
    Jiao, Long R.
    SURGERY, 2012, 152 (05) : 936 - 938
  • [20] Epstein-Barr Virus miR-BART6-3p Inhibits the RIG-I Pathway
    Lu, Yuanjun
    Qin, Zailong
    Wang, Jia
    Zheng, Xiang
    Lu, Jianhong
    Zhang, Xuemei
    Wei, Lingyu
    Peng, Qiu
    Zheng, Ying
    Ou, Chunlin
    Ye, Qiurong
    Xiong, Wei
    Li, Guiyuan
    Fu, Yuxin
    Yan, Qun
    Ma, Jian
    JOURNAL OF INNATE IMMUNITY, 2017, 9 (06) : 574 - 586