Evidence map›Paper›PMID 26918943›Full record

ArticleOncotarget2016

MicroRNA-30a increases tight junction protein expression to suppress the epithelial-mesenchymal transition and metastasis by targeting Slug in breast cancer.

Chia-Wei Chang, Jyh-Cherng Yu, Yi-Hsien Hsieh, Chung-Chin Yao, Jui-I Chao, Po-Ming Chen, Hsiao-Yen Hsieh, Chia-Ni Hsiung, Hou-Wei Chu, Chen-Yang Shen and 1 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 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.2field-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

33 citing papers in PubMed, 56 citations in OpenAlex.

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  16. MiR-30a suppresses metastasis of gastric adenocarcinoma via targeting FAPα.Cancer biomarkers : section A of Disease markers · 2020
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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 5 institutions in 1 country.

Chia-Wei ChangInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Jyh-Cherng YuDepartment of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Yi-Hsien HsiehInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chung-Chin YaoDepartment of Surgery, Chung Shan Medical University Hospital, Taichung, Taiwan.
Jui-I ChaoDepartment of Biological Science and Technology, National Chiao Tung University, Hsinchu, Taiwan.
Po-Ming ChenInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Hsiao-Yen HsiehInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chia-Ni HsiungInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Hou-Wei ChuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Chen-Yang ShenInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Chun-Wen ChengInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWInstitute of Biomedical Sciences, Academia Sinica · TWChung Shan Medical University Hospital · TWNational Defense Medical Center · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial-to-mesenchymal (EMT) transition is a prerequisite for conferring metastatic potential during tumor progression. microRNA-30a (miR-30a) expression was significantly lower in aggressive breast cancer cell lines compared with non-invasive breast cancer and non-malignant mammary epithelial cell lines. In contrast, miR-30a overexpression reversed the mesenchymal appearance of cancer cells to result in a cobblestone-like epithelial phenotype. We identified Slug, one of the master regulators of EMT, as a target of miR-30a using in silico prediction. Reporter assays indicated that miR-30a could bind to the 3'-untranslted region of Slug mRNA. Furthermore, we linked miR-30a to increased expression of claudins, a family of tight junction transmembrane proteins. An interaction between Slug and E-box in the claudin promoter sequences was reduced upon miR-30a overexpression, further leading to reduction of filopodia formation and decreased invasiveness/metastasis capabilities of breast cancer cells. Consistently, delivery of miR-30a in xenografted mice decreased tumor invasion and migration. In patients with breast cancer, a significantly elevated risk of the miR-30alow/CLDN2low/FSCNhigh genotype was observed, linking to a phenotypic manifestation of larger tumor size, lymph node metastasis, and advanced tumor stage among patients. In conclusion, the miR-30a/Slug axis inhibits mesenchymal tumor development by interfering with metastatic cancer cell programming and may be a potential target for therapy in breast cancer.

Indexed as

3' Untranslated RegionsAnimalsBreast NeoplasmsCell LineCell Line, TumorClaudinsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMice, Inbred BALB CMice, NudeMicroRNAsMicroscopy, ConfocalNeoplasm Metastasis3' Untranslated RegionsClaudinsMicroRNAsMIRN30b microRNA, humanSNAI1 protein, humanSnail Family Transcription FactorsTight Junction Proteinsbreast cancer metastasisclaudinEMTmiR-30aslug

Identifiers

PMID26918943
PMCPMC4941328
OpenAlexW2290724668

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.