Evidence map›Paper›PMID 32631390›Full record

ArticleBMC cancer2020

NR2F2 plays a major role in insulin-induced epithelial-mesenchymal transition in breast cancer cells.

Baili Xia, Lijun Hou, Huan Kang, Wenhui Chang, Yi Liu, Yanli Zhang, Yi Ding

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  8. Cellular heterogeneity and dynamics of the human uterus in healthy premenopausal women.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

7 authors at 1 institution in 1 country.

Baili XiaDepartment of Pathophysiology, Weifang Medical University, Weifang, 261053, China.
Lijun HouDepartment of Pathophysiology, Weifang Medical University, Weifang, 261053, China.
Huan KangDepartment of Pathophysiology, Weifang Medical University, Weifang, 261053, China.
Wenhui ChangDepartment of Pathophysiology, Weifang Medical University, Weifang, 261053, China.
Yi LiuDepartment of Pathophysiology, Weifang Medical University, Weifang, 261053, China.
Yanli ZhangDepartment of Pathophysiology, Weifang Medical University, Weifang, 261053, China.
Yi DingDepartment of Pathophysiology, Weifang Medical University, Weifang, 261053, China. dingyi6767@163.com.ORCID http://orcid.org/0000-0002-6201-0509
Weifang Medical University · CN

Funding

Department of Education of Shandong Province (CN) J13LK02Natural Science Foundation of China No.81472489
6 · The paper itself

Abstract

backgroundThe failure of treatment for breast cancer usually results from distant metastasis in which the epithelial-mesenchymal transition (EMT) plays a critical role. Hyperinsulinemia, the hallmark of Type 2 diabetes mellitus (T2DM), has been regarded as a key risk factor for the progression of breast cancer. Nuclear receptor subfamily 2, group F, member 2 (NR2F2) has been implicated in the development of breast cancer, however its contribution to insulin-induced EMT in breast cancer remains unclear.

methodsOverexpression and knockdown of NR2F2 were used in two breast cancer cell lines, MCF-7 and MDA-MB-231 to investigate potential mechanisms by which NR2F2 leads to insulin-mediated EMT. To elucidate the effects of insulin and signaling events following NR2F2 overexpression and knockdown, Cells' invasion and migration capacity and changes of NR2F2, E-cadherin, N-cadherin and vimentin were investigated by real-time RT-PCR and western blot.

resultsInsulin stimulation of these cells increased NR2F2 expression levels and promoted cell invasion and migration accompanied by alterations in EMT-related molecular markers. Overexpression of NR2F2 and NR2F2 knockdown demonstrated that NR2F2 expression was positively correlated with cell invasion, migration and the expression of N-cadherin and vimentin. In contrast, NR2F2 had an inverse correlation with E-cadherin expression. In MDA-MB-231, both insulin-induced cell invasion and migration and EMT-related marker alteration were abolished by NR2F2 knockdown.

conclusionsThese results suggest that NR2F2 plays a critical role in insulin-mediated breast cancer cell invasion, migration through its effect on EMT.

Indexed as

Breast NeoplasmsCell MovementCOUP Transcription Factor IIDiabetes Mellitus, Type 2Epithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHyperinsulinismInsulinMCF-7 CellsNeoplasm InvasivenessRisk FactorsCOUP Transcription Factor IIInsulinNR2F2 protein, humanBreast cancerEpithelial-mesenchymal transitionInsulinInvasion metastasisMigrationNR2F2

Identifiers

PMID32631390
PMCPMC7336611
OpenAlexW3038643635

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.