Evidence map›Paper›PMID 20370918›Full record

ArticleBMC cancer2010

The RNA binding protein HuR differentially regulates unique subsets of mRNAs in estrogen receptor negative and estrogen receptor positive breast cancer.

Robert Calaluce, Matthew M Gubin, J Wade Davis, Joseph D Magee, Jing Chen, Yuki Kuwano, Myriam Gorospe, Ulus Atasoy

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. HuR ablation destabilizesFrontiers in immunology · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The RNA-Binding Protein HuR in Digestive System Tumors.BioMed research international · 2020
    Review
  14. Article
  15. RNA regulons in cancer and inflammation.Current opinion in genetics & development · 2018
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

8 authors at 3 institutions in 1 country.

Robert CalaluceDepartment of Surgery, University of Missouri, Columbia, Missouri 65212, USA.
Matthew M Gubin
J Wade Davis
Joseph D Magee
Jing Chen
Yuki Kuwano
Myriam Gorospe
Ulus Atasoy
University of Missouri Hospital · USNational Institute on Aging · USUniversity of Missouri · US

Funding

Post-transcriptional Regulation Of Proliferative and Stress Response GenesZIAAG000511 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$25.4M
RNA-Binding Proteins that Modulate Proliferative and Stress-Response GenesZIAAG000392 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2010
$1.1M
6 · The paper itself

Abstract

backgroundThe discordance between steady-state levels of mRNAs and protein has been attributed to posttranscriptional control mechanisms affecting mRNA stability and translation. Traditional methods of genome wide microarray analysis, profiling steady-state levels of mRNA, may miss important mRNA targets owing to significant posttranscriptional gene regulation by RNA binding proteins (RBPs).

methodsThe ribonomic approach, utilizing RNA immunoprecipitation hybridized to microarray (RIP-Chip), provides global identification of putative endogenous mRNA targets of different RBPs. HuR is an RBP that binds to the AU-rich elements (ARE) of labile mRNAs, such as proto-oncogenes, facilitating their translation into protein. HuR has been shown to play a role in cancer progression and elevated levels of cytoplasmic HuR directly correlate with increased invasiveness and poor prognosis for many cancers, including those of the breast. HuR has been described to control genes in several of the acquired capabilities of cancer and has been hypothesized to be a tumor-maintenance gene, allowing for cancers to proliferate once they are established.

resultsWe used HuR RIP-Chip as a comprehensive and systematic method to survey breast cancer target genes in both MCF-7 (estrogen receptor positive, ER+) and MDA-MB-231 (estrogen receptor negative, ER-) breast cancer cell lines. We identified unique subsets of HuR-associated mRNAs found individually or in both cell types. Two novel HuR targets, CD9 and CALM2 mRNAs, were identified and validated by quantitative RT-PCR and biotin pull-down analysis.

conclusionThis is the first report of a side-by-side genome-wide comparison of HuR-associated targets in wild type ER+ and ER- breast cancer. We found distinct, differentially expressed subsets of cancer related genes in ER+ and ER- breast cancer cell lines, and noted that the differential regulation of two cancer-related genes by HuR was contingent upon the cellular environment.

Indexed as

Gene Expression Regulation, NeoplasticAntigens, CDAntigens, SurfaceBiotinBreast NeoplasmsCalmodulinCell Line, TumorELAV-Like Protein 1ELAV ProteinsHumansImmunoprecipitationMembrane GlycoproteinsOligonucleotide Array Sequence AnalysisReceptors, EstrogenRNA-Binding ProteinsRNA, MessengerAntigens, CDAntigens, SurfaceBiotinCALM2 protein, humanCalmodulinCD9 protein, humanELAVL1 protein, humanELAV-Like Protein 1ELAV ProteinsMembrane GlycoproteinsReceptors, EstrogenRNA-Binding ProteinsRNA, MessengerTetraspanin 29

Identifiers

PMID20370918
PMCPMC2856550
OpenAlexW2157502876

What OpenQuestion holds

Textmetadata
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.