PMID- 30317672
OWN - NLM
STAT- MEDLINE
DCOM- 20200720
LR  - 20211204
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 120
IP  - 4
DP  - 2019 Apr
TI  - MicroRNA-105 promotes epithelial-mesenchymal transition of nonsmall lung cancer 
      cells through upregulating Mcl-1.
PG  - 5880-5888
LID - 10.1002/jcb.27873 [doi]
AB  - BACKGROUND: A growing number of microRNAs have been proved to play significant 
      roles in limiting tumor growth and the epithelial-mesenchymal transition (EMT) 
      process of nonsmall cell lung cancer (NSCLC). Present work aims to study the 
      function of microRNA (miR)-105 in EMT of NSCLC cells, which is unrevealed yet. 
      METHODS: Two NSCLC cell lines A549 and Calu-3 were transfected with miR-105 
      mimic, inhibitor, or scrambled control. And then the effects of miR-105 were 
      evaluated by performing trypan blue staining, transwell assay, 
      ANNEXIN-FITC/propidium iodide (PI) double staining and Western blot analysis. The 
      expression levels of myeloid cell leukemia-1 (Mcl-1) after transfection were 
      tested by real-time quantitative polymerase chain reaction and Western blot 
      analysis. Whether Mcl-1 was a downstream effector of miR-105, and the involvement 
      of mammalian target of Rapamycin (mTOR) and p38 mitogen-activated protein kinase 
      (p38MAPK) signaling pathways were assessed. RESULTS: The overexpression of 
      miR-105 significantly increased the viability and migration of A549 and Calu-3, 
      but had no impacts on cell apoptosis. Meanwhile, E-cadherin was remarkably 
      downregulated, and N-cadherin, Vimentin, ZEB1, and Snail were upregulated by 
      miR-105 overexpression. Mcl-1 was positively regulated by miR-105, and the 
      effects of miR-105 overexpression on A549 and Calu-3 cells viability, migration 
      and EMT were all flattened by Mcl-1 silence. Both mTOR and p38MAPK pathways were 
      activated in miR-105-overexpressing and Mcl-1-overexpressing cells. Besides, 
      inhibition of mTOR and p38MAPK pathways by using Rapamycin and VX-702 abolished 
      the regulatory effects of Mcl-1 on EMT. CONCLUSION: Our study underlines the 
      importance of miR-105 in modulating NSCLC cells EMT. miR-105 promoted the EMT of 
      NSCLC cells possibly via upregulation of Mcl-1 and thereby activation of mTOR and 
      p38MAPK signaling.
CI  - (c) 2018 Wiley Periodicals, Inc.
FAU - Jin, Xiangfeng
AU  - Jin X
AD  - Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Yu, Yi
AU  - Yu Y
AD  - Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Zou, Qiang
AU  - Zou Q
AD  - Department of Blood Transfusion, Qingdao Haici Hospital Affiliated to Qingdao 
      University, Qingdao, China.
FAU - Wang, Mingzhao
AU  - Wang M
AD  - Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Cui, Yaojie
AU  - Cui Y
AD  - Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Xie, Jing
AU  - Xie J
AD  - Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Wang, Zizong
AU  - Wang Z
AUID- ORCID: 0000-0001-9998-7711
AD  - Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20181014
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (MCL1 protein, human)
RN  - 0 (MIRN105 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Myeloid Cell Leukemia Sequence 1 Protein)
RN  - 0 (Snail Family Transcription Factors)
RN  - 0 (Vimentin)
RN  - 0 (ZEB1 protein, human)
RN  - 0 (Zinc Finger E-box-Binding Homeobox 1)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
RIN - J Cell Biochem. 2021 Nov;122 Suppl 1:S34. PMID: 34101243
MH  - A549 Cells
MH  - Blotting, Western
MH  - Carcinoma, Non-Small-Cell Lung/genetics/*metabolism
MH  - Cell Line, Tumor
MH  - Epithelial-Mesenchymal Transition/genetics/*physiology
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Lung Neoplasms/genetics/*metabolism
MH  - MicroRNAs/genetics/*metabolism
MH  - Myeloid Cell Leukemia Sequence 1 Protein/genetics/metabolism
MH  - Snail Family Transcription Factors/genetics/metabolism
MH  - TOR Serine-Threonine Kinases/genetics/metabolism
MH  - Vimentin/genetics/metabolism
MH  - Zinc Finger E-box-Binding Homeobox 1/genetics/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/genetics/metabolism
OTO - NOTNLM
OT  - Mcl-1
OT  - epithelial-mesenchymal transition (EMT)
OT  - microRNA-105
OT  - nonsmall cell lung cancer (NSCLC)
EDAT- 2018/10/15 06:00
MHDA- 2020/07/21 06:00
CRDT- 2018/10/15 06:00
PHST- 2018/07/24 00:00 [received]
PHST- 2018/09/20 00:00 [accepted]
PHST- 2018/10/15 06:00 [pubmed]
PHST- 2020/07/21 06:00 [medline]
PHST- 2018/10/15 06:00 [entrez]
AID - 10.1002/jcb.27873 [doi]
PST - ppublish
SO  - J Cell Biochem. 2019 Apr;120(4):5880-5888. doi: 10.1002/jcb.27873. Epub 2018 Oct 
      14.