Evidence map›Paper›PMID 26023734›Full record

ArticleOncotarget2015

ERα inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer.

Xiao-Long Wei, Xiao-Wei Dou, Jing-Wen Bai, Xiang-Rong Luo, Si-Qi Qiu, Di-Di Xi, Wen-He Huang, Cai-Wen Du, Kwan Man, Guo-Jun Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 23 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

10 authors at 4 institutions in 2 countries.

Xiao-Long WeiDepartment of Pathology, Cancer Hospital of Shantou University Medical College, Shantou 515031, China.
Xiao-Wei DouChangjiang Scholar's Laboratory and Cancer Research Center, Shantou University Medical College, Shantou 515031, China.
Jing-Wen BaiChangjiang Scholar's Laboratory and Cancer Research Center, Shantou University Medical College, Shantou 515031, China.
Xiang-Rong LuoChangjiang Scholar's Laboratory and Cancer Research Center, Shantou University Medical College, Shantou 515031, China.
Si-Qi QiuThe Breast Center, Cancer Hospital of Shantou University Medical College, Shantou 515031, China.
Di-Di XiChangjiang Scholar's Laboratory and Cancer Research Center, Shantou University Medical College, Shantou 515031, China.
Wen-He HuangThe Breast Center, Cancer Hospital of Shantou University Medical College, Shantou 515031, China.
Cai-Wen DuDepartment of Breast Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, China.
Kwan ManDepartment of Surgery and Transplantation, Li Ka Shing Faculty of Medicine, Hong Kong University, Hong Kong 999077, China.
Guo-Jun ZhangChangjiang Scholar's Laboratory and Cancer Research Center, Shantou University Medical College, Shantou 515031, China.
Shantou University Medical College · CNShantou University · CNCancer Hospital of Shantou University Medical College · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In human breast cancer, estrogen receptor-α (ERα) suppresses epithelial-mesenchymal transition (EMT) and stemness, two crucial parameters for tumor metastasis; however, the underlying mechanism by which ERα regulates these two processes remains largely unknown. Bmi1, the polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog, regulates EMT transition, maintains the self-renewal capacity of stem cells, and is frequently overexpressed in human cancers. In the present study, ERα upregulated the expression of the epithelial marker, E-cadherin, in breast cancer cells through the transcriptional down-regulation of Bmi1. Furthermore, ERα overexpression suppressed the migration, invasion, and EMT of breast cancer cells. Notably, overexpression of ERα significantly decreased the CD44high/CD24low cell population and inhibited the capacity for mammosphere formation in ERα-negative breast cancer cells. In addition, overexpression of Bmi1 attenuated the ERα-mediated suppression of EMT and cell stemness. Immunohistochemistry revealed an inverse association of ERα and Bmi1 expression in human breast cancer tissue. Taken together, our findings suggest that ERα inhibits EMT and stemness through the downregulation of Bmi1.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCadherinsCD24 AntigenCell MovementEstrogen Receptor alphaEstrogensFemaleHumansHyaluronan ReceptorsImmunohistochemistryMiceMice, Inbred BALB CMice, NudeBMI1 protein, humanCadherinsCD24 AntigenCD44 protein, humanESR1 protein, humanEstrogen Receptor alphaEstrogensHyaluronan ReceptorsPolycomb Repressive Complex 1Bmi1breast cancerepithelial-mesenchymal transitionERα signalingstemness

Identifiers

PMID26023734
PMCPMC4673297
OpenAlexW1739900546

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.