Evidence map›Paper›PMID 32313093›Full record

ArticleScientific reports2020

UTMD inhibit EMT of breast cancer through the ROS/miR-200c/ZEB1 axis.

Dandan Shi, Lu Guo, Xiao Sun, Mengmeng Shang, Dong Meng, Xiaoying Zhou, Xinxin Liu, Yading Zhao, Jie Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
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  8. Article
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  12. Self-Reinforced Bimetallic Mito-Jammer for CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  13. Article
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  15. Review
  16. Article
  17. Article
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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 at 1 institution in 1 country.

Dandan ShiDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Lu GuoDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Xiao SunDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Mengmeng ShangDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Dong MengDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Xiaoying ZhouDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Xinxin LiuDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Yading ZhaoDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China.
Jie LiDepartment of ultrasound, Qilu Hospital of Shandong University, Jinan, 250012, China. jieli301@163.com.
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a potential drug/gene delivery system, the ultrasound-targeted microbubble destruction (UTMD) system can be used as a vehicle as well as increasing the permeability of biological barriers to enhance the effect of tumor treatment. However, the effect of UTMD in the tumor EMT process is unknown. In this study, we aimed to investigate the potential and mechanism of UTMD induced oxidative stress in inhibiting EMT of breast cancer. Human breast MDA231 cells were treated with microbubble (MB), ultrasound (US) and UTMD, respectively. The generation of oxidative stress, the levels of miR-200c, ZEB1 and vimentin, and the numbers of migratory cells were evaluated quantitatively and qualitatively by the measurement of intracellular reactive oxygen species (ROS), qRT-PCR, western blot assay, and transwell assay. Then, to evaluate the role of UTMD-induced oxidative stress and miR-200c in the epithelial-mesenchymal transition (EMT) inhibition, the ROS scavenger N-acetyl-L-cysteine (NAC) and miR-200c inhibitor were used before UTMD treatment. We found that UTMD induced oxidative stress, upregulated the expression of miR-200c, downregulated the expression of ZEB1 and vimentin and suppressed the MDA231 cell migration. The addition of NAC and miR-200c inhibitor had an opposite impact on the expression of miR-200c and ZEB1, thus hindered the effects of UTMD on MDA231 cells EMT. In conclusion, UTMD can inhibit the EMT characteristics of MDA231 cells. The mechanism may be related to the regulation of the miR-200c/ZEB1 axis through the generation of ROS induced by UTMD, which may provide a new strategy to prevent the tumor cells EMT under UTMD treatment.

Indexed as

Gene Expression Regulation, NeoplasticAcetylcysteineCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleFree Radical ScavengersGene Transfer TechniquesHumansMammary Glands, HumanMicrobubblesMicroRNAsOxidative StressReactive Oxygen SpeciesRNA, Small InterferingAcetylcysteineFree Radical ScavengersMicroRNAsMIRN200 microRNA, humanReactive Oxygen SpeciesRNA, Small InterferingVimentinVIM protein, humanZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID32313093
PMCPMC7170845
OpenAlexW3016454700

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.