Evidence map›Paper›PMID 26522726›Full record

ArticleOncogene2016

mTORC1 directly phosphorylates and activates ERα upon estrogen stimulation.

A Alayev, R S Salamon, S M Berger, N S Schwartz, R Cuesta, R B Snyder, M K Holz

Abstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Current insight into the molecular mechanisms of lymphangioleiomyomatosis.American journal of respiratory cell and molecular biology · 2026
    Review
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  11. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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4 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

A AlayevDepartment of Biology, Yeshiva University, New York, NY, USA.
R S SalamonDepartment of Biology, Yeshiva University, New York, NY, USA.
S M BergerDepartment of Biology, Yeshiva University, New York, NY, USA.
N S SchwartzDepartment of Biology, Yeshiva University, New York, NY, USA.
R CuestaDepartment of Biology, Yeshiva University, New York, NY, USA.
R B SnyderDepartment of Biology, Yeshiva University, New York, NY, USA.
M K HolzDepartment of Biology, Yeshiva University, New York, NY, USA.
Yeshiva University · USAlbert Einstein College of Medicine · US

Funding

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 CA151112
6 · The paper itself

Abstract

Breast cancer is the leading cause of cancer-related deaths among women. Approximately 75% of breast cancers are estrogen receptor-α (ERα) positive, underscoring the dependence of cancer cells on estrogen for growth and survival. Patients treated with endocrine therapy often develop resistance, either de novo or acquired, which in some cases is caused by aberrations within the growth factor signaling pathways. The mechanistic target of rapamycin complex 1 (mTORC1) has emerged as a critical node in estrogenic signaling. We have previously shown that mTORC1 can phosphorylate and activate ERα on S167 via its effector-the 40S ribosomal S6 kinase 1 (S6K1). Presently, we have uncovered a direct link between mTORC1 and ERα. We found that ERα binds to regulatory-associated protein of mTOR (Raptor) and causes it to translocate to the nucleus upon estrogen stimulation. In addition, we identified mTOR as the kinase that phosphorylates ERα on S104/106 and activates transcription of ER target genes. Our findings show a direct link between mTORC1 and ERα, which further implicates mTORC1 signaling in the pathogenesis of ER-positive breast cancer and provides rationale for FDA-approved use of mTORC1 inhibitors in combination with endocrine agents for treatment of this disease.

Indexed as

Active Transport, Cell NucleusAdaptor Proteins, Signal TransducingBreast NeoplasmsCell Line, TumorCell NucleusEstrogen AntagonistsEstrogen Receptor alphaEstrogensGene Expression Regulation, NeoplasticHEK293 CellsHumansMCF-7 CellsMechanistic Target of Rapamycin Complex 1Microscopy, FluorescenceMultiprotein ComplexesPhosphorylationAdaptor Proteins, Signal TransducingESR1 protein, humanEstrogen AntagonistsEstrogen Receptor alphaEstrogensMechanistic Target of Rapamycin Complex 1MTOR protein, humanMultiprotein ComplexesRegulatory-Associated Protein of mTORRPTOR protein, humanSerineTamoxifenTOR Serine-Threonine Kinases

Identifiers

PMID26522726
PMCPMC4853282
OpenAlexW2234248432

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.