PMID- 29275213
OWN - NLM
STAT- MEDLINE
DCOM- 20181029
LR  - 20181029
IS  - 1878-5875 (Electronic)
IS  - 1357-2725 (Linking)
VI  - 95
DP  - 2018 Feb
TI  - Overexpression of miR-1290 contributes to cell proliferation and invasion of non 
      small cell lung cancer by targeting interferon regulatory factor 2.
PG  - 113-120
LID - S1357-2725(17)30330-8 [pii]
LID - 10.1016/j.biocel.2017.12.017 [doi]
AB  - MicroRNAs are small endogenous non-coding RNAs, which can frequently emerge as 
      regulators in many cancer types. MiR-1290 was found to be abnormally elevated in 
      non small cell lung cancer (NSCLC). However, the underlying molecular mechanism 
      still needs to be investigated. Here, we demonstrated that miR-1290 expression 
      levels were remarkably upregulated in NSCLC tissues compared to adjacent normal 
      tissues. Higher miR-1290 expression levels positively associated with lymph node 
      metastasis and advanced tumor stage. Functional assays showed that upregulated 
      miR-1290 expression in NSCLC cells enhanced cell proliferation, cell colony 
      formation and invasion capacities in vitro. Furthermore, we found that miR-1290 
      promoted cell proliferation related protein CDK2 and CDK4 expression and enhanced 
      Epithelial-Mesenchymal Transition (EMT) process by downregulating E-cadherin 
      expression and upregulating N-cadherin expression. Bioinformatics analysis and 
      luciferase reporter gene assays revealed that Interferon regulatory factor 2 
      (IRF2) was a direct target of miR-1290. Overexpression of miR-1290 can degrade 
      IRF2 mRNA and downregulated IRF2 protein expression in NSCLC cells. Upregulated 
      IRF2 could partly rescue the promoting effects induced by miR-1290 overexpression 
      on cell proliferation and invasion of NSCLC. Additionally, we confirmed that 
      reduced miR-1290 expression could suppress tumor growth using a tumor xenograft 
      model in vivo. Thus, we concluded that miR-1290 may serve as a potential target 
      of NSCLC treatment.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Jin, Jian-Jun
AU  - Jin JJ
AD  - Department of Respiratory and Critical Medicine, The First Affiliated Hospital of 
      Zhengzhou University, Zhengzhou 450052, Henan Province, China.
FAU - Liu, Yuan-Hua
AU  - Liu YH
AD  - Department of Respiratory and Critical Medicine, The First Affiliated Hospital of 
      Zhengzhou University, Zhengzhou 450052, Henan Province, China.
FAU - Si, Ji-Ming
AU  - Si JM
AD  - Department of Respiratory and Critical Medicine, The First Affiliated Hospital of 
      Zhengzhou University, Zhengzhou 450052, Henan Province, China.
FAU - Ni, Ran
AU  - Ni R
AD  - Department of Respiratory and Critical Medicine, The First Affiliated Hospital of 
      Zhengzhou University, Zhengzhou 450052, Henan Province, China.
FAU - Wang, Jing
AU  - Wang J
AD  - Department of Respiratory and Critical Medicine, The First Affiliated Hospital of 
      Zhengzhou University, Zhengzhou 450052, Henan Province, China. Electronic 
      address: wangjing197701@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171221
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - 0 (Antagomirs)
RN  - 0 (IRF2 protein, human)
RN  - 0 (Interferon Regulatory Factor-2)
RN  - 0 (MIRN1290 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (RNA, Neoplasm)
RN  - 0 (RNA, recombinant)
RN  - 0 (Recombinant Proteins)
RN  - 63231-63-0 (RNA)
SB  - IM
MH  - Aged
MH  - Animals
MH  - Antagomirs/therapeutic use
MH  - Carcinoma, Non-Small-Cell Lung/*metabolism/pathology/therapy
MH  - Cell Line, Tumor
MH  - Epithelial-Mesenchymal Transition
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Interferon Regulatory Factor-2/*antagonists & inhibitors/genetics/metabolism
MH  - Lung/*metabolism/pathology
MH  - Lung Neoplasms/*metabolism/pathology/therapy
MH  - Male
MH  - Mice, Nude
MH  - MicroRNAs/*metabolism
MH  - Middle Aged
MH  - Neoplasm Invasiveness/pathology/prevention & control
MH  - Neoplasm Proteins/*antagonists & inhibitors/genetics/metabolism
MH  - RNA/antagonists & inhibitors/metabolism
MH  - RNA, Neoplasm/metabolism
MH  - RNAi Therapeutics
MH  - Recombinant Proteins/chemistry/metabolism
MH  - Xenograft Model Antitumor Assays
OTO - NOTNLM
OT  - Interferon regulatory factor 2
OT  - MicroRNA
OT  - Non small cell lung cancer
OT  - Tumor progression
OT  - miR-1290
EDAT- 2017/12/25 06:00
MHDA- 2018/10/30 06:00
CRDT- 2017/12/25 06:00
PHST- 2017/09/24 00:00 [received]
PHST- 2017/12/16 00:00 [revised]
PHST- 2017/12/19 00:00 [accepted]
PHST- 2017/12/25 06:00 [pubmed]
PHST- 2018/10/30 06:00 [medline]
PHST- 2017/12/25 06:00 [entrez]
AID - S1357-2725(17)30330-8 [pii]
AID - 10.1016/j.biocel.2017.12.017 [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 2018 Feb;95:113-120. doi: 10.1016/j.biocel.2017.12.017. 
      Epub 2017 Dec 21.