Evidence map›Paper›PMID 22787161›Full record

ArticleThe Journal of biological chemistry2012

p53, a target of estrogen receptor (ER) α, modulates DNA damage-induced growth suppression in ER-positive breast cancer cells.

Crystal E Berger, Yingjuan Qian, Gang Liu, Hongwu Chen, Xinbin Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

54 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026
    Article
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  14. Molecules (Basel, Switzerland) · 2024
    Article
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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

5 authors at 3 institutions in 1 country.

Crystal E BergerComparative Oncology Laboratory, University of California, Davis, CA 95616, USA.
Yingjuan Qian
Gang Liu
Hongwu Chen
Xinbin Chen
University of California, Davis · USUC Davis Comprehensive Cancer CenterUniversity of Alabama at Birmingham · US

Funding

Mechanism of p53-Mediated Tumor SuppressionR01CA076069 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2002 to 2017
$4.5M
MECHANISM OF P53 DEPENDENT APOPTOSISR29CA076069 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, XINBIN · 1998 to 2002
$276k
NCI NIH HHS CA076069NCI NIH HHS R01 CA076069NCI NIH HHS R29 CA076069
6 · The paper itself

Abstract

In response to genotoxic stress, the p53 tumor suppressor induces target genes for cell cycle arrest, apoptosis, and DNA repair. Although p53 is the most commonly mutated gene in all human cancers, it is only mutated in about 20% of breast cancers. 70% of all breast cancer cases are estrogen receptor (ER)-positive and express ERα. ER-positive breast cancer generally indicates good patient prognosis and treatment responsiveness with antiestrogens, such as tamoxifen. However, ER-positive breast cancer patients can experience loss or a reduction in ERα, which is associated with aggressive tumor growth, increased invasiveness, poor prognosis, and loss of p53 function. Consistent with this, we found that p53 is a target gene of ERα. Specifically, we found that knockdown of ERα decreases expression of p53 and its downstream targets, MDM2 and p21. In addition, we found that ERα activates p53 transcription via binding to estrogen response element half-sites within the p53 promoter. Moreover, we found that loss of ERα desensitizes, whereas ectopic expression of ERα sensitizes, breast cancer cells to DNA damage-induced growth suppression in a p53-dependent manner. Altogether, this study provides an insight into a feedback loop between ERα and p53 and a biological role of p53 in the DNA damage response in ER-positive breast cancers.

Indexed as

DNA DamageGene Expression Regulation, NeoplasticBreast NeoplasmsCell Line, TumorDNA, NeoplasmEstrogen Receptor alphaFemaleGene Knockdown TechniquesHumansProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53DNA, NeoplasmESR1 protein, humanEstrogen Receptor alphaMDM2 protein, humanProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22787161
PMCPMC3436267
OpenAlexW1969790866

What OpenQuestion holds

Textmetadata
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.