Evidence map›Paper›PMID 30830488›Full record

ArticleBreast cancer research and treatment2019

ERα upregulates the expression of long non-coding RNA LINC00472 which suppresses the phosphorylation of NF-κB in breast cancer.

Zhanwei Wang, Dionyssios Katsaros, Nicoletta Biglia, Yi Shen, Lenora Loo, Xiao Yu, Hongyan Lin, Yuanyuan Fu, Wen-Ming Chu, Peiwen Fei and 5 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Breast cancer research and treatment, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-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

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  4. Metformin and long non-coding RNAs in breast cancer.Journal of translational medicine · 2023
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  19. Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1.Cancer biomarkers : section A of Disease markers · 2021
    Article
  20. Review
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

15 authors at 2 institutions in 2 countries.

Zhanwei WangUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Dionyssios KatsarosDepartment of Surgical Sciences, Gynecology, AOU Città della Salute, University of Torino, Turin, Italy.
Nicoletta BigliaDivision of Obstetrics and Gynecology, Department of Surgical Sciences, University of Torino School of Medicine, Mauriziano Hospital, Turin, Italy.
Yi ShenUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Lenora LooUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Xiao YuHongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, 227 South Chongqing Road, Shanghai, 200025, China.
Hongyan LinHongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, 227 South Chongqing Road, Shanghai, 200025, China.
Yuanyuan FuUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Wen-Ming ChuUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Peiwen FeiUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Yan NiUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Wei JiaUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
Xiaobei DengHongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, 227 South Chongqing Road, Shanghai, 200025, China.
Biyun QianHongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, 227 South Chongqing Road, Shanghai, 200025, China. qianbiyun@shsmu.edu.cn.
Herbert YuUniversity of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA. hyu@cc.hawaii.edu.ORCID http://orcid.org/0000-0003-3950-4815
University of Hawaiʻi at Mānoa · USShanghai Jiao Tong University · CN

Funding

Epidemiologic Study of Hepatocellular Carcinoma in the USR01CA138698 · NCI · YALE UNIVERSITY · PI YU, HERBERT · 2010 to 2015
$5.7M
Molecular Insights into the Fanconi Anemia Tumor Suppressor Signaling PathwayR01CA188251 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI FEI, PEIWEN · 2014 to 2018
$1.6M
NCI NIH HHS R01 CA138698NCI NIH HHS R01 CA188251
6 · The paper itself

Abstract

purposeLow expression of long intergenic non-coding RNA LINC00472 in breast cancer is associated with aggressive tumors and unfavorable disease outcomes in multiple clinical datasets, but the reasons for these associations were unknown.

methodsTo study the mechanisms underlying the lncRNA's connection to breast cancer, we investigated the molecular targets and regulation of LINC00472 in breast cancer cells, and analyzed relevant molecular features in relation to patient survival. Gene expression profiles of breast cancer cells overexpressing LINC00472 were analyzed for its regulatory pathways and downstream targets. Effects of LINC00472 overexpression on cell behaviors were evaluated in vitro and in vivo. Meta-analysis was performed using online datasets and our own study.

resultsAnalysis of LINC00472 transcriptome revealed ERα upregulation of LINC00472 expression, and an ERα-binding site in the LINC00472 promoter was identified. Evaluation of LINC00472 overexpression also indicated a possible link between LINC00472 and NF-κB. Cell experiments confirmed that LINC00472 suppressed the phosphorylation of p65 and IκBα through binding to IKKβ, inhibiting its phosphorylation. High LINC00472 expression inhibited tumor growth both in vitro and in vivo and suppressed aggressive tumor cell behaviors in vitro. Suppressing LINC00472 expression in ER-positive tumor cells increased cell aggressive behaviors. Tamoxifen treatment of ER-positive cells inhibited ERα and LINC00472 expression and increased p65 and IκBα phosphorylation. Meta-analysis showed that LINC00472 expression were higher in ER-positive than ER-negative tumors and that high expression was associated with better disease outcomes in ER-positive patients.

conclusionsThe study demonstrates that ERα upregulates LINC00472 which suppresses the phosphorylation of NF-κB, and suggests that endocrine treatment may lower LINC00472 and increase NF-κB activities, leading to tumor progression and disease recurrence.

Indexed as

AdultAgedAged, 80 and overAnimalsBreast NeoplasmseIF-2 KinaseEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHeterograftsHumansMCF-7 CellsMiceMiddle AgedNeoplasm Recurrence, LocalNF-kappa BeIF-2 KinaseESR1 protein, humanEstrogen Receptor alphaLINC00472 RNA, humanNF-kappa BRNA, Long NoncodingTamoxifenBreast cancerEndocrine resistanceERαLINC00472LncRNANF-κBPrognosis

Identifiers

PMID30830488
PMCPMC6534447
OpenAlexW2920286628

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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.