The Key microRNAs Regulated the Development of Non-small Cell Lung Cancer by Targeting TGF-β-induced epithelial–mesenchymal Transition
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Published:2019-07-24
Issue:4
Volume:22
Page:238-244
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ISSN:1386-2073
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Container-title:Combinatorial Chemistry & High Throughput Screening
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language:en
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Short-container-title:CCHTS
Affiliation:
1. Department of General Surgery, Deqing People’s Hospital, Huzhou 313200, China 2. Department of Thoracic Surgery, Hangzhou Red Cross Hospital, Hangzhou 310003, China
Abstract
Purpose:
Epithelial-to-Mesenchymal Transition (EMT) was reported to play a key role
in the development of Non-Small Cell Lung Cancer (NSCLC). The process of EMT is regulated by
the changes of miRNAs expression. However, it is still unknown which miRNA changed the most
in the process of canceration and whether these changes played a role in tumor development.
Methods:
A total of 36 SCLC patients treated in our hospital between 11th, 2015 and 10th, 2017
were enrolled. The samples of cancer tissues and paracancer tissues of patients were collected and
analyzed. Then, the miRNAs in normal lung cells and NSCLC cells were also analyzed. In the
presence of TGF-β, we transfected the miRNA mimics or inhibitor into NSCLC cells to investigate
the role of the significantly altered miRNAs in cell migration and invasion and in the process of
EMT.
Results:
MiR-330-3p was significantly up-regulated in NSCLC cell lines and tissues and miRNA-
205 was significantly down-regulated in NSCLC cell lines and NSCLC tissues. Transfected
miRNA-205 mimics or miRMA-330-3p inhibitor inhibited the migration and invasion of NCIH1975
cell and restrained TGF-β-induced EMT in NSCLC cells.
Conclusion:
miRNA-330-3p and miRNA-205 changed the most in the process of canceration in
NSCLC. Furthermore, miR-330-3p promoted cell invasion and metastasis in NSCLC probably by
promoting EMT and miR-205 could restrain NSCLC likely by suppressing EMT.
Publisher
Bentham Science Publishers Ltd.
Subject
Organic Chemistry,Computer Science Applications,Drug Discovery,General Medicine
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