Evidence map›Paper›PMID 27049344›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Estrogen receptor alpha is cell cycle-regulated and regulates the cell cycle in a ligand-dependent fashion.

Sonia JavanMoghadam, Zhang Weihua, Kelly K Hunt, Khandan Keyomarsi

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ESR1 Regulates Fecundity and Functions in Sheep Endometrial Stromal Cells.International journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. The Role of Estrogen across Multiple Disease Mechanisms.Current issues in molecular biology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. 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

4 authors at 2 institutions in 1 country.

Sonia JavanMoghadama Department of Experimental Radiation Oncology , The University of Texas MD Anderson Cancer Center , Houston , TX , USA.
Zhang Weihuab Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
Kelly K Huntc Department of Breast Surgical Oncology , The University of Texas MD Anderson Cancer Center , Houston , TX , USA.
Khandan Keyomarsia Department of Experimental Radiation Oncology , The University of Texas MD Anderson Cancer Center , Houston , TX , USA.
The University of Texas MD Anderson Cancer Center · USUniversity of Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Estrogen receptor alpha (ERα) has been implicated in several cell cycle regulatory events and is an important predictive marker of disease outcome in breast cancer patients. Here, we aimed to elucidate the mechanism through which ERα influences proliferation in breast cancer cells. Our results show that ERα protein is cell cycle-regulated in human breast cancer cells and that the presence of 17-β-estradiol (E2) in the culture medium shortened the cell cycle significantly (by 4.5 hours, P < 0.05) compared with unliganded conditions. The alterations in cell cycle duration were observed in the S and G2/M phases, whereas the G1 phase was indistinguishable under liganded and unliganded conditions. In addition, ERα knockdown in MCF-7 cells accelerated mitotic exit, whereas transfection of ERα-negative MDA-MB-231 cells with exogenous ERα significantly shortened the S and G2/M phases (by 9.1 hours, P < 0.05) compared with parental cells. Finally, treatment of MCF-7 cells with antiestrogens revealed that tamoxifen yields a slower cell cycle progression through the S and G2/M phases than fulvestrant does, presumably because of the destabilizing effect of fulvestrant on ERα protein. Together, these results show that ERα modulates breast cancer cell proliferation by regulating events during the S and G2/M phases of the cell cycle in a ligand-dependent fashion. These results provide the rationale for an effective treatment strategy that includes a cell cycle inhibitor in combination with a drug that lowers estrogen levels, such as an aromatase inhibitor, and an antiestrogen that does not result in the degradation of ERα, such as tamoxifen.

Indexed as

Gene Expression Regulation, NeoplasticAphidicolinCell Line, TumorCell ProliferationEstradiolEstrogen AntagonistsEstrogen Receptor alphaFemaleFulvestrantG1 PhaseG2 Phase Cell Cycle CheckpointsHumansLigandsLovastatinMCF-7 CellsRNA, Small InterferingAphidicolinESR1 protein, humanEstradiolEstrogen AntagonistsEstrogen Receptor alphaFulvestrantLigandsLovastatinRNA, Small InterferingTamoxifenbreast neoplasmscell cycleestradiolEstrogen receptor alphareceptor modulatorsselective estrogen

Identifiers

PMID27049344
PMCPMC4934046
OpenAlexW2329662673

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.