Evidence map›Paper›PMID 27929537›Full record

ArticleCell death & disease2016

Upregulation of MiR-205 under hypoxia promotes epithelial-mesenchymal transition by targeting ASPP2.

Xingwen Wang, Miao Yu, Kunming Zhao, Mengmeng He, Wenjie Ge, Yuhui Sun, Yihua Wang, Haizhu Sun, Ying Hu

Abstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

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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

9 authors.

Xingwen WangSchool of Life Science and Technology, Harbin Institute of Technology, Shenzhen, China.
Miao YuSchool of Chemical Engineering and Technology, Harbin Institute of Technology, Harbin, China.
Kunming ZhaoSchool of Life Science and Technology, Harbin Institute of Technology, Shenzhen, China.
Mengmeng HeSchool of Life Science and Technology, Harbin Institute of Technology, Shenzhen, China.
Wenjie GeSchool of Life Science and Technology, Harbin Institute of Technology, Shenzhen, China.
Yuhui SunThe First Affiliated Hospital, Harbin Medical University, Harbin, China.
Yihua WangBiological Sciences, Faculty of Natural and Environmental Sciences, University of Southampton, Southampton, UK.ORCID 0000-0001-5561-0648
Haizhu SunThe Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Ying HuSchool of Life Science and Technology, Harbin Institute of Technology, Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) is one of the crucial procedures for cancer invasion and distal metastasis. Despite undergoing intensive studies, the mechanisms underlying EMT remain to be completely elucidated. Here, we identified that apoptosis-stimulating protein of p53-2 (ASPP2) is a novel target of MiR-205 in various cancers. Interestingly, the binding site of MiR-205 at the 3'-untranslated region of ASPP2 was highly conserved among different species. An inverse correlation between MiR-205 and ASPP2 was further observed in vivo in cervical cancers, suggesting MiR-205 may be an important physiological inhibitor of ASPP2. Hypoxia is a hallmark of solid tumor microenvironment and one of such conditions to induce EMT. Notably, MiR-205 was remarkably induced by hypoxia in cervical and lung cancer cells. A marked suppression of ASPP2 was observed simultaneously. Further studies confirmed that hypoxia-induced ASPP2 suppression was mainly attributed to the elevated MiR-205. Interestingly, the alteration of MiR-205/ASPP2 under hypoxia was accompanied with the decreased epithelial marker E-cadherin and increased mesenchymal marker Vimentin, as well as a morphological transition from the typical cobblestone-like appearance to the mesenchymal-like structure. More importantly, MiR-205 mimics or ASPP2 silencing similarly promoted EMT process. By contrast, ASPP2 recovery or MiR-205 inhibitor reversed MiR-205-dependent EMT. Further studies demonstrated that the newly revealed MiR-205/ASPP2 axis promoted cell migration and also increased cell proliferation both in vivo and in vitro. These data together implicated a critical impact of MiR-205/ASPP2 on promoting EMT. MiR-205/ASPP2 may be potential diagnostic and therapeutic biomarkers in cervical and lung cancers.

Indexed as

AnimalsApoptosis Regulatory ProteinsBase SequenceCell HypoxiaCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMice, NudeMicroRNAsModels, BiologicalSignal TransductionUp-RegulationApoptosis Regulatory ProteinsMicroRNAsMIR205, humanTP53BP2 protein, human

Identifiers

PMID27929537
PMCPMC5261019

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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.