Evidence map›Paper›PMID 28956730›Full record

ArticleCancer biology & therapy2017

Inactivation of miR-100 combined with arsenic treatment enhances the malignant transformation of BEAS-2B cells via stimulating epithelial -mesenchymal transition.

Jia Yang, Zhijun Chen, Xinyi Wang, Mo Xu, Haoshu Fang, Feifei Li, Yakun Liu, Yu Jiang, Yi Ding, Juan Li and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer biology & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

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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 3 institutions in 1 country.

Jia Yanga Department of Anesthesia, School of Medicine , Shandong University , Jinan , Shandong , China.
Zhijun Chenb Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.
Xinyi Wangb Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.
Mo Xub Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.
Haoshu Fangb Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.
Feifei Lib Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.
Yakun Liub Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.
Yu Jiangb Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.
Yi Dingc Department of Pathology and Physiology , Weifang Medical College , Weifang , Shandong , China.
Juan Lia Department of Anesthesia, School of Medicine , Shandong University , Jinan , Shandong , China.
Siying Wangb Department of Pathophysiology, School of Basic Medical Science, Affiliated Anhui Provincial Hospital , Anhui Medical University , Hefei , Anhui , China.ORCID http://orcid.org/0000-0003-4793-7389
Anhui Medical University · CNShandong University · CNWeifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic arsenic treatment induces epithelial-mesenchymal transition (EMT) and promotes tumorigenicity, but the mechanism is unclear. MiR-100 has been shown to be involved in this biologic process. In this study, we hypothesize that inactivation of miR-100 combined with low concentration of arsenic exposure could promote the malignant transformation of human bronchial epithelial cells (BEAS-2B cell) by promoting EMT. To test this hypothesis, BEAS-2B cells were treated with low-dose of As

Indexed as

AnimalsArsenicBronchiCarcinogenesisCell MovementCell ProliferationCell Transformation, NeoplasticEpithelial CellsEpithelial-Mesenchymal TransitionHeterograftsHumansMiceMicroRNAsSignal TransductionArsenicMicroRNAsMIRN100 microRNA, humanCarcinogenesislung cancermicro RNAmiR-100

Identifiers

PMID28956730
PMCPMC5718807
OpenAlexW2759123409

What OpenQuestion holds

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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.