Evidence map›Paper›PMID 28727734›Full record

ArticlePloS one2017

MicroRNA-200c inhibits epithelial-mesenchymal transition, invasion, and migration of lung cancer by targeting HMGB1.

Po-Len Liu, Wei-Lun Liu, Jia-Ming Chang, Yung-Hsiang Chen, Yu-Peng Liu, Hsuan-Fu Kuo, Chong-Chao Hsieh, Yu-Sian Ding, Wei-Wei Chen, Inn-Wen Chong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 67 citations in OpenAlex.

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  5. MicroRNA-200c in Cancer Generation, Invasion, and Metastasis.International journal of molecular sciences · 2025
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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

10 authors at 5 institutions in 1 country.

Po-Len LiuDepartment of Respiratory Therapy, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.ORCID http://orcid.org/0000-0003-2896-1666
Wei-Lun LiuDepartment of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan.
Jia-Ming ChangPreclinical Animal Pharmacology Testing Center, National Research Project for Biopharmaceuticals, New Taipei, Taiwan.
Yung-Hsiang ChenGraduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan.
Yu-Peng LiuDepartment of Genome Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Hsuan-Fu KuoDepartment of Internal Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Chong-Chao HsiehDivision of Cardiovascular Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Yu-Sian DingPreclinical Animal Pharmacology Testing Center, National Research Project for Biopharmaceuticals, New Taipei, Taiwan.
Wei-Wei ChenPreclinical Animal Pharmacology Testing Center, National Research Project for Biopharmaceuticals, New Taipei, Taiwan.
Inn-Wen ChongDepartment of Respiratory Therapy, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Kaohsiung Medical University · TWDevelopment Center for Biotechnology · TWAsia University · TWFu Jen Catholic University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRs) play critical roles in cancer development, proliferation, epithelial-mesenchymal transition (EMT), invasion, and migration through regulating the expression of oncogenes and tumour suppressor genes. Previous studies have indicated that miR-200c acts as a tumour suppressor in various cancers by downregulating high-mobility group box 1 (HMGB1) and thereby suppressing EMT and metastasis. In addition, miR-200c was reported to be downregulated and correlated with poor outcomes in non-small cell lung cancer (NSCLC). However, its functional role in HMGB1 regulation in NSCLC is still unclear. This study aimed to clarify whether miR-200c acts as a tumour suppressor in NSCLC by downregulating HMGB1, which is associated with EMT, invasion, cytoskeleton rearrangement, and migration in vitro and in vivo. In order to demonstrate HMGB1 downregulation by miR-200c, the NSCLC cell line A549 was transfected with miR-200c mimic or inhibitor. The mimic significantly reduced HMGB1 expression and suppressed EMT, invasion, and migration, while the inhibitor generated the opposite effects. Additionally, using xenograft mouse models, we confirmed that HMGB1 overexpression increased tumour EMT. In summary, our results demonstrated that miR-200c could suppress EMT, invasion, and migration of NSCLC cells by downregulating HMGB1.

Indexed as

AdenocarcinomaAnimalsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHeterograftsHMGB1 ProteinHumansLungLung NeoplasmsMiceMicroRNAsNeoplasm InvasivenessNeoplasm TransplantationRNA, Small InterferingHMGB1 ProteinMicroRNAsMIRN200 microRNA, humanRNA, Small Interfering

Identifiers

PMID28727734
PMCPMC5519074
OpenAlexW2738947042

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.