Evidence map›Paper›PMID 26837415›Full record

ArticleActa biochimica et biophysica Sinica2016

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting EYA2.

Yuncang Yuan, Shangyong Zheng, Qian Li, Xudong Xiang, Tangxin Gao, Pengzhan Ran, Lijuan Sun, Qionglin Huang, Fei Xie, Jing Du and 1 more

Abstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 33 citations in OpenAlex.

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  8. miR-4732-5p promotes breast cancer progression by targeting TSPAN13.Journal of cellular and molecular medicine · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Yuncang YuanSchool of Medicine, Yunnan University, Kunming 650091, China.
Shangyong ZhengSchool of Medicine, Yunnan University, Kunming 650091, China.
Qian LiSchool of Medicine, Yunnan University, Kunming 650091, China.
Xudong XiangDepartment of Thoracic Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming 650118, China.
Tangxin GaoSchool of Medicine, Yunnan University, Kunming 650091, China.
Pengzhan RanSchool of Medicine, Yunnan University, Kunming 650091, China.
Lijuan SunSchool of Medicine, Yunnan University, Kunming 650091, China.
Qionglin HuangSchool of Medicine, Yunnan University, Kunming 650091, China.
Fei XieSchool of Medicine, Yunnan University, Kunming 650091, China.
Jing DuSchool of Medicine, Yunnan University, Kunming 650091, China.
Chunjie XiaoSchool of Medicine, Yunnan University, Kunming 650091, China chjxiao@ynu.edu.cn.
Yunnan University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

3' Untranslated RegionsAdenocarcinomaCell Line, TumorDown-RegulationHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMicroRNAsNeoplasm InvasivenessNeoplasm MetastasisNuclear ProteinsProtein Tyrosine Phosphatases3' Untranslated RegionsEYA2 protein, humanIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN30b microRNA, humanNuclear ProteinsProtein Tyrosine PhosphatasesEYA2invasionlung adenocarcinomamigrationmiR-30a

Identifiers

PMID26837415
PMCPMC4885132
OpenAlexW2266834609

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.