Evidence map›Paper›PMID 12370804›Full record

ArticleOncogene2002

A role for TGF-beta in estrogen and retinoid mediated regulation of the nuclear receptor coactivator AIB1 in MCF-7 breast cancer cells.

Kristina J Lauritsen, Heinz-Joachim List, Ronald Reiter, Anton Wellstein, Anna T Riegel

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Review
  3. SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021
    Review
  4. Differential recruitment of co-regulatory proteins to the human estrogen receptor 1 in response to xenoestrogens.Comparative biochemistry and physiology. Part D, Genomics & proteomics · 2016
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Estrogen down-regulation of the corepressor N-CoR: mechanism and implications for estrogen derepression of N-CoR-regulated genes.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  15. Coactivator AIB1 links estrogen receptor transcriptional activity and stability.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  16. Review
  17. 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

5 authors at 2 institutions in 1 country.

Kristina J LauritsenDepartment of Oncology, Vincent T Lombardi Cancer Center, Research Building, E307, Georgetown University, 3970 Reservoir Road, Washington, DC 20007, USA.
Heinz-Joachim List
Ronald Reiter
Anton Wellstein
Anna T Riegel
Georgetown University · USGeorgetown University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AIB1 (amplified in breast cancer 1) is a nuclear receptor coactivator gene amplified and overexpressed in breast cancer. However, the mechanisms by which AIB1 is regulated are unclear. Here we show that 17beta-estradiol represses AIB1 mRNA and protein expression in MCF-7 human breast cancer cells primarily by suppressing AIB1 gene transcription. Estrogen levels present in fetal calf serum are sufficient to maintain AIB1 mRNA and protein at low basal levels, and this repression is reversed by the addition of antiestrogens or all-trans retinoic acid. Interestingly, cycloheximide inhibition experiments revealed that secondary protein synthesis was necessary to induce AIB1 expression by antiestrogens and retinoids. Experiments with TGF-beta and TGF-beta blocking antibodies demonstrated that this growth factor modulates AIB1 expression and showed that the antiestrogen and retinoid induction of AIB1 gene expression is mediated at least in part through TGF-beta. These data reveal a mechanism of estrogen-induced down-modulation of the overall hormone sensitivity of cells through feedback inhibition of coactivator gene expression. These data also suggest that antiestrogens can shift the sensitivity of cells to non-estrogenic proliferative signaling by increasing cellular levels of AIB1. This effect may play a role in breast cancer progression and resistance to drug treatment.

Indexed as

Gene Expression Regulation, NeoplasticBreast NeoplasmsCell CycleEstradiolFulvestrantHalf-LifeHumansNuclear Receptor Coactivator 3RNA, MessengerTranscription FactorsTransforming Growth Factor betaTretinoinTumor Cells, CulturedEstradiolFulvestrantNuclear Receptor Coactivator 3RNA, MessengerTranscription FactorsTransforming Growth Factor betaTretinoin

Identifiers

PMID12370804
OpenAlexW2000306281

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.