Evidence map›Paper›PMID 25734775›Full record

ArticlePloS one2015

Role of Bmi-1 in regulation of ionizing irradiation-induced epithelial-mesenchymal transition and migration of breast cancer cells.

Weiwei Yuan, Ye Yuan, Tao Zhang, Shiyong Wu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Effects of radiation on the metastatic process.Molecular medicine (Cambridge, Mass.) · 2018
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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

4 authors at 3 institutions in 2 countries.

Weiwei YuanDepartment of Oncology, the General Hospital of Chengdu Military District, Chengdu, Sichuan, P. R. China; Department of Chemistry and Biochemistry, and Edison Biotechnology Institute, Ohio University, Athens, Ohio, 45701, United States of America.
Ye YuanDepartment of Chemistry and Biochemistry, and Edison Biotechnology Institute, Ohio University, Athens, Ohio, 45701, United States of America.
Tao ZhangDepartment of Oncology, the General Hospital of Chengdu Military District, Chengdu, Sichuan, P. R. China.
Shiyong WuDepartment of Chemistry and Biochemistry, and Edison Biotechnology Institute, Ohio University, Athens, Ohio, 45701, United States of America.
Ohio University · USBiotechnology Institute · USChengdu Military General Hospital · CN

Funding

UV INDUCED AND PERK MEDIATED SIGNALING PATHWAYSR01CA086928 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WU, SHIYONG · 2000 to 2012
$2.1M
NCI NIH HHS R01 CA086928NCI NIH HHS R01CA086928
6 · The paper itself

Abstract

Radiotherapy is a widely used treatment for cancer. However, recent studies suggest that ionizing radiation (IR) can promote tumor invasion and metastasis. Bmi-1, a member of the polycomb group protein family, has been observed as a regulator of oxidative stress and promotes metastasis in some tumors. But, its potential role in the metastasis induced by IR of breast cancer has not been explored. In our study, we found that increased levels of Bmi-1 were correlated to EMT of breast cancer cells. Through analyzing the EMT state and metastasis of breast cancer induced by IR, we found the metastatic potential of breast cancer cells can either be inhibited or accelerated by IR following a time-dependent pattern. Silencing Bmi-1 completely abolished the ability of the IR to alter, reduce or increase, the migration of breast cancer cells. Also, when Bmi-1 was knocked down, the effect of inhibition of PI3K/AKT signaling on EMT affected by IR was blocked. These results suggest that Bmi-1 is a key gene in regulation of EMT and migration of breast cancer cells induced by IR through activation of PI3K/AKT signaling; therefore, Bmi-1 could be a new target for inhibiting metastasis caused by IR.

Indexed as

Radiation, IonizingBreast NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleHumansMCF-7 CellsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPolycomb Repressive Complex 1Proto-Oncogene Proteins c-aktRNA InterferenceRNA, Small InterferingSignal TransductionBMI1 protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPolycomb Repressive Complex 1Proto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID25734775
PMCPMC4348174
OpenAlexW2065103413

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.