Evidence map›Paper›PMID 23250869›Full record

ArticleHormones & cancer2013

A MicroRNA196a2* and TP63 circuit regulated by estrogen receptor-α and ERK2 that controls breast cancer proliferation and invasiveness properties.

Kyuri Kim, Zeynep Madak-Erdogan, Rosa Ventrella, Benita S Katzenellenbogen

Open access · bronzeAbstract read
In one paragraph

Article in Hormones & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. The Role of Estrogen in Brain MicroRNAs Regulation.Advanced pharmaceutical bulletin · 2024
    Review
  4. How MicroRNAs Command the Battle against Cancer.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Therapeutic Targeting of MicroRNAs in the Tumor Microenvironment.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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  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

4 authors at 1 institution in 1 country.

Kyuri KimDepartment of Molecular and Integrative Physiology, University of Illinois and College of Medicine at Urbana-Champaign, Urbana, IL 61801, USA.
Zeynep Madak-Erdogan
Rosa Ventrella
Benita S Katzenellenbogen
University of Illinois Urbana-Champaign · US

Funding

Research Training Program in Toxicology and Environmental HealthT32ES007326 · NIEHS · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI Jodi A. Flaws · 2000 to 2026
$8.7M
Pharmacokinetics, Bioavailability, and Metabolism/Daniel R. DoergeP50AT006268 · NCCIH · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI HELFERICH, WILLIAM G · 2010 to 2015
$7.6M
NCCIH NIH HHS P50 AT006268NIEHS NIH HHS T32 ES007326NIEHS NIH HHS T32ES007326
6 · The paper itself

Abstract

Estrogen receptor α (ERα) is present in about 70 % of human breast cancers and, working in conjunction with extracellular signal-regulated kinase 2 (ERK2), this nuclear hormone receptor regulates the expression of many protein-encoding genes. Given the crucial roles of miRNAs in cancer biology, we investigated the regulation of miRNAs by estradiol (E2) through ERα and ERK2, and their impact on target gene expression and phenotypic properties of breast cancer cells. We identified miRNA-encoding genes harboring overlapping ERα and ERK chromatin binding sites in ERα-positive MCF-7 cells and showed ERα and ERK2 to bind to these sites and to be required for transcriptional induction of these miRNAs by E2. Hsa-miR-196a2*, the most highly estrogen up-regulated miRNA, markedly down-regulated tumor protein p63 (TP63), a member of the p53 family. In ERα-positive and ERα-negative breast cancer cells, proliferative and invasiveness properties were suppressed by hsa-miR-196a2* expression and enhanced by hsa-miR-196a2* antagonism or TP63 target protector oligonucleotides. Hsa-miR-196a2* and TP63 were inversely correlated in breast cancer cell lines and in a large cohort of human breast tumors, implying clinical relevance. The findings reveal a tumor suppressive role of hsa-miR-196a2* through regulation of TP63 by ERα and/or ERK2 signaling. Manipulating the hsa-miR-196a2*-TP63 axis might provide a potential tumor-suppressive strategy to alleviate the aggressive behavior and poor prognosis of some ERα-positive as well as many ERα-negative breast cancers.

Indexed as

Breast NeoplasmsCell ProliferationEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsMitogen-Activated Protein Kinase 1Neoplasm InvasivenessSignal TransductionTranscription FactorsTumor Suppressor ProteinsEstrogen Receptor alphaMAPK1 protein, humanMicroRNAsMIRN196 microRNA, humanMitogen-Activated Protein Kinase 1TP63 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID23250869
PMCPMC3581735
OpenAlexW2053739452

What OpenQuestion holds

Textmetadata
LicenceTDM
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.