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Abstract |
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| Vol 48 No. 3: 220-228 |
[PDF] [Full Text] |
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| Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting EYA2 |
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| Yuncang Yuan1,†,
Shangyong Zheng1,†,
Qian Li1,
Xudong Xiang2,
Tangxin Gao1,
Pengzhan Ran1,
Lijuan Sun1,
Qionglin Huang1,
Fei Xie1,
Jing Du1 and
Chunjie Xiao1,*
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1School of Medicine, Yunnan University, Kunming 650091, China
2Department of Thoracic Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming 650118, China
† These authors contributed equally to this work. |
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Abstract MicroRNAs (miRNAs) are a class of small non-coding RNAs and closely related to the pathogenesis of cancers. Increasing evidence indicates that miR-30a plays a profound role during the development of cancers. However, the functions of miR-30a in non-small-cell lung cancer (NSCLC) are still ambiguous. Here we found that miR-30a was decreased in lung adenocarcinoma A549 cells and in tissue samples from 14 patients by qRT-PCR, and also found that overexpression of miR-30a in A549 cells inhibited migration and invasion but not cell proliferation and cell cycle progression by wound-healing assay, matrigel invasion assay, MTS-based cell proliferation assay, and flow cytometry-based cell cycle analysis, respectively. We further explored the potential mechanism of miR-30a-mediated gene regulation in lung adenocarcinoma cell lines. EYA2 is a predicted target of miR-30a, and it has been found that EYA2 expression is inhibited by miR-30a in breast cancer cells. We demonstrated that EYA2 is a direct target of miR-30a by using the dual-luciferase reporter assay in A549 cells and showed that EYA2 protein levels are inversely correlated with miR-30a expression in A549 and BEAS-2B cells. In addition, we also confirmed the rescue effects of EYA2 overexpression in A549 cells by cotransfection with EYA2 expression vector and miR-30a mimics. Taken together, our results demonstrate that overexpression of miR-30a in lung adenocarcinoma A549 cells can inhibit cell migration and invasion, which is partially attributed to the decrease of EYA2 expression. Our findings suggest that miR-30a may be used as a new potential target for the treatment of lung adenocarcinoma in the future. |
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Keywords lung adenocarcinoma; miR-30a; migration; invasion; EYA2 |
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Received 2015-6-23
Accepted 2015-11-23 |
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Funding This work was supported by the grants from the National Natural Science Foundation of China (Nos. 81372360 and 81460435) and the Key Projects of Applied Basic Research of Yunnan Province (No. 2014FA022). |
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* Correspondence address Tel: +86-13888455098; Fax: +86-871-65034636; E-mail: [email protected] |
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