MiR‐5702 suppresses proliferation and invasion in non‐small‐cell lung cancer cells via posttranscriptional suppression of ZEB1
MiRNAs have emerged as important players in tumorigenesis and progression. MiR‐5702 is a newly identified miRNA; the exact role of which has not been reported. Here, we found that miR‐5702 was significantly decreased in the carcinoma tissues of non‐small cell lung cancer (NSCLC) patients and NSCLC c...
Saved in:
Published in | Journal of biochemical and molecular toxicology Vol. 32; no. 7; pp. e22163 - n/a |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.07.2018
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | MiRNAs have emerged as important players in tumorigenesis and progression. MiR‐5702 is a newly identified miRNA; the exact role of which has not been reported. Here, we found that miR‐5702 was significantly decreased in the carcinoma tissues of non‐small cell lung cancer (NSCLC) patients and NSCLC cell lines. Then, our results showed that the miR‐5702 mimic induced apoptosis and inhibited proliferation and invasion in A549 cells. In contrast, the miR‐5702 inhibitor reduced apoptosis and increased proliferation and invasion in A549 cells. Furthermore, bioinformatics and 3′‐UTR luciferase reporter assays identified that oncogene zinc finger E‐box‐binding homeobox 1 (ZEB1) is a target gene of miR‐5702. Western blotting analysis showed that miR‐5702 overexpression suppressed, and miR‐5702 knockdown promoted the expression of ZEB1 protein. Finally, the ZEB1 siRNA exhibited a similar effect to the miR‐5702 mimic on expression of ZEB1 and its downstream genes, cell apoptosis, cell proliferation, and cell invasion, and it could antagonize the alternations in ZEB1 expression and cell behaviors by the miR‐5702 inhibitor. In conclusion, miR‐5702 may function as a tumor suppressor in NSCLC, which suppresses proliferation and invasion NSCLC cells via posttranscriptional suppression of ZEB1. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1095-6670 1099-0461 |
DOI: | 10.1002/jbt.22163 |