Evidence map›Paper›PMID 27223073›Full record

ArticleOncotarget2016

MicroRNA-138 acts as a tumor suppressor in non small cell lung cancer via targeting YAP1.

Ling Xiao, Hui Zhou, Xiang-Ping Li, Juan Chen, Chao Fang, Chen-Xue Mao, Jia-Jia Cui, Wei Zhang, Hong-Hao Zhou, Ji-Ye Yin and 1 more

RetractedOpen access · diamondAbstract readRetracted Publication
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

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  13. lncRNA PFAR Promotes Lung Fibroblast Activation and Fibrosis by Targeting miR-138 to Regulate the YAP1-Twist Axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Ling XiaoDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Hui ZhouThe Affiliated Cancer Hospital, XiangYa School of Medicine, Central South University, Changsha, Hunan 410014, P.R. China.
Xiang-Ping LiDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Juan ChenDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Chao FangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Chen-Xue MaoDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Jia-Jia CuiDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Wei ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Hong-Hao ZhouDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Ji-Ye YinDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Zhao-Qian LiuDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Hunan 410078, P.R. China.
Xiangya Hospital Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA (miR)-138 was found to have suppressive effects on the growth and metastasis of different human cancers. In this study, we aimed to investigate the regulatory mechanism of miR-138 in non-small cell lung cancer (NSCLC). We applied the Quantitative real-time PCR (qRT-PCR) to detect the miR-138 levels in NSCLC tissues (n=21) and cell lines, Bioinformatical predication, luciferase reporter assay and western blot to identify the target gene of miR-138. We also applied Cell transfection, MTT, transwell, and wound healing assays to reveal the role of miR-138 in NSCLC cell proliferation and malignant transformation. We observed that miR-138 expression level was significantly decreased in NSCLC tissues compared to their matched adjacent normal tissues. It was also downregulated in tissues with poor differentiation, advanced stage or lymph nodes metastasis, as well as in several NSCLC cell lines compared to normal lung epithelial cell. We further identified YAP1 as a direct target gene of miR-138, and observed that the protein level of YAP1 was negatively mediated by miR-138 in NSCLC A549 cells. Moreover, overexpression of miR-138 significantly inhibited A549 cell growth, invasion and migration, while knockdown of miR-138 enhanced such capacities. Further investigation showed that the cell proliferation capacity was higher in the miR-138+YAP1 group, when compared with that in the miR-138 group, suggesting that overexpression of YAP1 rescued the suppressive effects of miR-138 upregulation on NSCLC cell proliferation. However, we found no difference of cell invasion and migration capacities between miR-138+YAP1 group and miR-138 group. Finally, YAP1 was markedly upregulated in NSCLC tissues compared to their marched adjacent normal tissues. Its mRNA levels were reversely correlated with the miR-138 levels in NSCLC tissues. In summary, our study suggests that miR-138 may play a suppressive role in the growth and metastasis of NSCLC cells partly at least by targeting YAP1.

Indexed as

Gene Expression Regulation, NeoplasticGenes, Tumor SuppressorA549 CellsAdaptor Proteins, Signal TransducingAgedCarcinoma, Non-Small-Cell LungCell DifferentiationCell Line, TumorCell MovementComputational BiologyFemaleHumansLung NeoplasmsMaleMicroRNAsMiddle AgedAdaptor Proteins, Signal TransducingMicroRNAsMIRN138 microRNA, humanPhosphoproteinsTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsgrowthmetastasismicroRNA-138non small cell lung cancerYes-associated protein 1

Identifiers

PMID27223073
PMCPMC5129990
OpenAlexW2406320186

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.