Over-expression of long non-coding RNA ZEB2-AS1 may predict poor prognosis and promote the migration, invasion, and epithelial-mesenchymal transition of tumor cells in non-small cell lung cancer
Background: Non-small cell lung cancer (NSCLC) remains the most common cause of human cancer-related death worldwide, and the present study aims to explore the roles of long non-coding (lnc)RNA ZEB2-AS1 in NSCLC and the related mechanism. Methods: Quantitative real-time-polymerase chain reaction was...
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Published in | The International journal of biological markers Vol. 35; no. 3; pp. 29 - 35 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London, England
SAGE Publications
01.09.2020
Sage Publications Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Background:
Non-small cell lung cancer (NSCLC) remains the most common cause of human cancer-related death worldwide, and the present study aims to explore the roles of long non-coding (lnc)RNA ZEB2-AS1 in NSCLC and the related mechanism.
Methods:
Quantitative real-time-polymerase chain reaction was performed to compare the expressions of ZEB2-AS1 in NSCLC cancer tissue and the adjacent non-tumorous tissues. The diagnostic and prognostic roles of ZEB2-AS1 in NSCLC were also evaluated by the receiver operating characteristic curve and the Kaplan–Meier survival analysis. NSCLC cell line A549 cells were transfected with ZEB2-AS1 siRNA, and the cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT) of the ZEB2-AS1 siRNA group and control group were compared.
Results:
ZEB2-AS1 was significantly increased in NSCLC tissues. The knockdown of ZEB2-AS1 markedly inhibited the cell viability, migration, invasion, and EMT of A549 cells in vitro.
Conclusion:
ZEB2-AS1 was up-regulated in NSCLC, and it may serve as a potential target for the diagnosis, prognosis, and treatment of NSCLC. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1724-6008 0393-6155 1724-6008 |
DOI: | 10.1177/1724600820938385 |