Evidence map›Paper›PMID 30573685›Full record

ArticleThe Journal of biological chemistry2019

Estrogen receptor α promotes protein synthesis by fine-tuning the expression of the eukaryotic translation initiation factor 3 subunit f (eIF3f).

Rafael Cuesta, Adi Y Berman, Anya Alayev, Marina K Holz

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. 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
1.2field-weighted citation impact, top 20% 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, 17 citations in OpenAlex.

  1. Review
  2. Foxg1 and companions: Not only transcription factors.Neural regeneration research · 2026
    Article
  3. Review
  4. Methylation marks breast cancer metastasis: The roles of mThe Journal of biological chemistry · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Unraveling the multifaceted nature of the nuclear function of mTOR.Biochimica et biophysica acta. Molecular cell research · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  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

4 authors at 3 institutions in 1 country.

Rafael CuestaFrom the Department of Cell Biology and Anatomy, New York Medical College, Valhalla, New York 10595.
Adi Y Bermanthe Department of Biology, Yeshiva University, New York, New York 10016, and.
Anya Alayevthe Department of Biology, Yeshiva University, New York, New York 10016, and.
Marina K HolzFrom the Department of Cell Biology and Anatomy, New York Medical College, Valhalla, New York 10595, mholz@nymc.edu.ORCID 0000-0001-5030-7973
Yeshiva University · USAlbert Einstein College of Medicine · USNew York Medical College · US

Funding

Estrogenic signaling upstream and downstream of mTORR35GM128675 · NIGMS · NEW YORK MEDICAL COLLEGE · PI HOLZ, MARINA K · 2018 to 2022
$2.4M
The role of the mTOR signaling pathway in ER-positive breast cancerR15CA151112 · NCI · YESHIVA UNIVERSITY · PI HOLZ, MARINA K · 2010 to 2013
$951k
NCI NIH HHS R15 CA151112NIGMS NIH HHS R35 GM128675
6 · The paper itself

Abstract

Approximately two thirds of all breast cancer cases are estrogen receptor (ER)-positive. The treatment of this breast cancer subtype with endocrine therapies is effective in the adjuvant and recurrent settings. However, their effectiveness is compromised by the emergence of intrinsic or acquired resistance. Thus, identification of new molecular targets can significantly contribute to the development of novel therapeutic strategies. In recent years, many studies have implicated aberrant levels of translation initiation factors in cancer etiology and provided evidence that identifies these factors as promising therapeutic targets. Accordingly, we observed reduced levels of the eIF3 subunit eIF3f in ER-positive breast cancer cells compared with ER-negative cells, and determined that low eIF3f levels are required for proper proliferation and survival of ER-positive MCF7 cells. The expression of eIF3f is tightly controlled by ERα at the transcriptional (genomic pathway) and translational (nongenomic pathway) level. Specifically, estrogen-bound ERα represses transcription of the

Indexed as

Gene Expression Regulation, NeoplasticSignal Transduction3' Untranslated RegionsBreast NeoplasmsCell ProliferationCell SurvivalEstrogen Receptor alphaEukaryotic Initiation Factor-3FemaleHumansMCF-7 CellsMechanistic Target of Rapamycin Complex 1Neoplasm Proteins3' Untranslated RegionsEIF3F protein, humanESR1 protein, humanEstrogen Receptor alphaEukaryotic Initiation Factor-3Mechanistic Target of Rapamycin Complex 1Neoplasm Proteinsbreast cancereIF3fERαestrogen receptoreukaryotic translation initiationgene expressionmTORC1translation

Identifiers

PMID30573685
PMCPMC6378971
OpenAlexW2905820046

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.