Evidence map›Paper›PMID 37695911›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

Serine starvation silences estrogen receptor signaling through histone hypoacetylation.

Albert M Li, Bo He, Dimitris Karagiannis, Yang Li, Haowen Jiang, Preethi Srinivasan, Yaniel Ramirez, Meng-Ning Zhou, Christina Curtis, Joshua J Gruber and 3 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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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

13 authors at 3 institutions in 1 country.

Albert M Li *Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-0865-6915
Bo He *Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0003-1471-9772
Dimitris KaragiannisDepartment of Genetics and Development, Columbia University Irving Medical Center, New York, NY 10032.
Yang LiDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-1914-5598
Haowen JiangDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0003-4021-3820
Preethi SrinivasanDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Yaniel RamirezDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.
Meng-Ning ZhouDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0001-8885-6089
Christina CurtisCancer Biology Program, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0003-0166-3802
Joshua J GruberDepartment of Internal Medicine, Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75235.
Chao LuDepartment of Genetics and Development, Columbia University Irving Medical Center, New York, NY 10032.
Erinn B RankinDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.
Jiangbin YeDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0003-1117-4869
Stanford University · USColumbia University Irving Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Translational Biology CoreP01CA257907 · NCI · STANFORD UNIVERSITY · PI Maximilian Diehn, Quynh-Thu Xuan Le · 2022 to 2026
$12.0M
MARC at University of California, DavisT34GM136469 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ALDRIN V. GOMES, Crystal D Rogers · 2020 to 2026
$2.8M
NCI NIH HHS P01 CA257907NCI NIH HHS T32 CA009302NIGMS NIH HHS T34 GM136469
6 · The paper itself

Abstract

Loss of estrogen receptor (ER) pathway activity promotes breast cancer progression, yet how this occurs remains poorly understood. Here, we show that serine starvation, a metabolic stress often found in breast cancer, represses estrogen receptor alpha (ERα) signaling by reprogramming glucose metabolism and epigenetics. Using isotope tracing and time-resolved metabolomic analyses, we demonstrate that serine is required to maintain glucose flux through glycolysis and the TCA cycle to support acetyl-CoA generation for histone acetylation. Consequently, limiting serine depletes histone H3 lysine 27 acetylation (H3K27ac), particularly at the promoter region of ER pathway genes including the gene encoding ERα,

Indexed as

Estrogen Receptor alphaHistonesAcetyl Coenzyme AGlucoseReceptors, EstrogenAcetyl Coenzyme AEstrogen Receptor alphaGlucoseHistonesReceptors, Estrogenbreast cancerestrogen receptorhistone acetylationserine metabolismSLC25A1

Identifiers

PMID37695911
PMCPMC10515173
OpenAlexW4386590156

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.