Evidence map›Paper›PMID 24441041›Full record

ArticleOncogene2014

The atypical ubiquitin ligase RNF31 stabilizes estrogen receptor α and modulates estrogen-stimulated breast cancer cell proliferation.

J Zhu, C Zhao, A Razavirad, T Zhuang, P Jonsson, N Liang, C Williams, C-Y Lin, Y Qiao, K Zendehdel and 3 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

65 citing papers in PubMed, 102 citations in OpenAlex.

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  18. Monoubiquitination in Homeostasis and Cancer.International journal of molecular sciences · 2022
    Review
  19. FKBP52 and FKBP51 differentially regulate the stability of estrogen receptor in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  20. Article

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 3 countries.

J ZhuDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
C ZhaoDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
A Razavirad1] Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden [2] Cancer Research Center, Cancer institute of Iran, Tehran University of Medical Sciences, Tehran, Iran.
T ZhuangDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
P JonssonCenter for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, TX, USA.
N LiangDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
C WilliamsCenter for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, TX, USA.
C-Y LinCenter for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, TX, USA.
Y QiaoDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
K ZendehdelCancer Research Center, Cancer institute of Iran, Tehran University of Medical Sciences, Tehran, Iran.
S StrömbladDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
E TreuterDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
K Dahlman-WrightDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Karolinska Institutet · SEUniversity of Houston · USMotamed Cancer Institute · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen receptor α (ERα) is initially expressed in the majority of breast cancers and promotes estrogen-dependent cancer progression by regulating the transcription of genes linked to cell proliferation. ERα status is of clinical importance, as ERα-positive breast cancers can be successfully treated by adjuvant therapy with antiestrogens or aromatase inhibitors. Complications arise from the frequent development of drug resistance that might be caused by multiple alterations, including components of ERα signaling, during tumor progression and metastasis. Therefore, insights into the molecular mechanisms that control ERα expression and stability are of utmost importance to improve breast cancer diagnostics and therapeutics. Here we report that the atypical E3 ubiquitin ligase RNF31 stabilizes ERα and facilitates ERα-stimulated proliferation in breast cancer cell lines. We show that depletion of RNF31 decreases the number of cells in the S phase and reduces the levels of ERα and its downstream target genes, including cyclin D1 and c-myc. Analysis of data from clinical samples confirms correlation between RNF31 expression and the expression of ERα target genes. Immunoprecipitation indicates that RNF31 associates with ERα and increases its stability and mono-ubiquitination, dependent on the ubiquitin ligase activity of RNF31. Our data suggest that association of RNF31 and ERα occurs mainly in the cytosol, consistent with the lack of RNF31 recruitment to ERα-occupied promoters. In conclusion, our study establishes a non-genomic mechanism by which RNF31 via stabilizing ERα levels controls the transcription of estrogen-dependent genes linked to breast cancer cell proliferation.

Indexed as

Cell ProliferationUbiquitinationBreast NeoplasmsCytosolEstradiolEstrogen Receptor alphaEstrogensFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansMCF-7 CellsProtein BindingProtein Interaction Domains and MotifsProtein StabilityProtein TransportESR1 protein, humanEstradiolEstrogen Receptor alphaEstrogensRNF31 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID24441041
PMCPMC4141304
OpenAlexW1968233052

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.