Evidence map›Paper›PMID 26919096›Full record

ArticleOncotarget2016

MiR-206 inhibits HGF-induced epithelial-mesenchymal transition and angiogenesis in non-small cell lung cancer via c-Met /PI3k/Akt/mTOR pathway.

Qing-yong Chen, De-min Jiao, Yu-quan Wu, Jun Chen, Jian Wang, Xia-li Tang, Hao Mou, Hui-zhen Hu, Jia Song, Jie Yan and 3 more

Open access · diamondAbstract read
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. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 115 citations in OpenAlex.

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  8. Angioregulatory microRNAs in breast cancerJournal of advanced research · 2022
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  13. MYOD1 inhibits avian adipocyte differentiation via miRNA-206/KLF4 axis.Journal of animal science and biotechnology · 2021
    Article
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7 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 2 countries.

Qing-yong ChenDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
De-min JiaoDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Yu-quan WuDepartment of Oncology, The 117th Hospital of PLA, Zhejiang, China.
Jun ChenDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Jian WangDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Xia-li TangDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Hao MouDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Hui-zhen HuDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Jia SongDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Jie YanDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Li-jun WuDepartment of Respiratory Disease, The 117th Hospital of PLA, Zhejiang, China.
Jianyan ChenDepartment of Anesthesiology, Shenzhen Baoan Hospital Affiliated to Southern Medical University, Guangdong, China.
Zhiwei WangDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Zhejiang Hospital · CNFirst Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiR-206 is low expression in lung cancers and associated with cancer metastasis. However, the roles of miR-206 in epithelial-mesenchymal transition (EMT) and angiogenesis in lung cancer remain unknown. In this study, we find that hepatocyte growth factor (HGF) induces EMT, invasion and migration in A549 and 95D lung cancer cells, and these processes could be markedly inhibited by miR-206 overexpression. Moreover, we demonstrate that miR-206 directly targets c-Met and inhibits its downstream PI3k/Akt/mTOR signaling pathway. In contrast, miR-206 inhibitors promote the expression of c-Met and activate the PI3k/Akt/mTOR signaling, and this effect could be attenuated by the PI3K inhibitor. Moreover, c-Met overexpression assay further confirms the significant inhibitory effect of miR-206 on HGF-induced EMT, cell migration and invasion. Notably, we also find that miR-206 effectively inhibits HGF-induced tube formation and migration of human umbilical vein endothelial cells (HUVECs), and the mechanism is also related to inhibition of PI3k/Akt/mTOR signaling. Finally, we reveal the inhibitory effect of miR-206 on EMT and angiogenesis in xenograft tumor mice model. Taken together, miR-206 inhibits HGF-induced EMT and angiogenesis in lung cancer by suppressing c-Met/PI3k/Akt/mTOR signaling. Therefore, miR-206 might be a potential target for the therapeutic strategy against EMT and angiogenesis of lung cancer.

Indexed as

A549 CellsAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHepatocyte Growth FactorHumansHuman Umbilical Vein Endothelial CellsLungLung NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsHepatocyte Growth FactorHGF protein, humanMET protein, humanMicroRNAsMIRN206 microRNA, humanMTOR protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metTOR Serine-Threonine Kinasesangiogenesisepithelial-mesenchymal transitionHGFlung cancermiR-206

Identifiers

PMID26919096
PMCPMC4951285
OpenAlexW2291930530

What OpenQuestion holds

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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.