Evidence mapPaperPMID 40665359Full record

ArticleBreast cancer research : BCR2025

Fibroblast growth factor receptor signaling modulates cholesterol storage in a SOAT1-dependent manner to promote mammary tumor cell invasion.

Jennifer E Tuokkola, Lyndsay E Reese, Ying Wang, Christine H O'Connor, Jillian G VanTreeck, Annisa H Rumahorbo, Kathryn L Schwertfeger

Abstract read
In one paragraph

Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
field-weighted citation impact
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

1 citing paper in PubMed.

  1. Breast Cancer Progression by the FGF/FGFR Axis: A Metabolic Perspective.Journal of mammary gland biology and neoplasia · 2025
    Review
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.

Jennifer E TuokkolaMolecular Pharmacology and Therapeutics Graduate Program, University of Minnesota, Minneapolis, MN, USA.
Lyndsay E ReeseDepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Ying WangDepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Christine H O'ConnorDepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Jillian G VanTreeckMolecular Pharmacology and Therapeutics Graduate Program, University of Minnesota, Minneapolis, MN, USA.
Annisa H RumahorboDepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Kathryn L SchwertfegerDepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA. schwe251@umn.edu.

Funding

Defining the contributions of Lyve-1 expressing macrophages to breast cancer growth and progressionR01CA265004 · UNIVERSITY OF MINNESOTA · 2025 to 2025
$415k
Contributions of FGFR-Mediated Tumor-Stromal Interactions to Breast Cancer Growth and ProgressionR01CA215052 · UNIVERSITY OF MINNESOTA · 2025 to 2025
$378k
NCI NIH HHS R01 CA215052NCI NIH HHS R01CA215052NCI NIH HHS R01 CA265004
6 · The paper itself

Abstract

Signaling by fibroblast growth factor receptors (FGFRs) is active in up to 85% of breast cancers and results in enhanced proliferation, migration, and invasion of tumor cells. Here, we show that FGFR signaling regulates cholesterol metabolism in breast cancer. Specifically, we demonstrate that FGFR activation promotes cellular cholesterol storage by upregulating expression of the enzyme sterol O-acyltransferase 1 (SOAT1). Moreover, we demonstrate that inhibition of SOAT1 attenuates FGFR-driven colony formation and invasion in tumor cells, which correlates with reduced expression of matrix metalloproteinase expression. Furthermore, genetic knockdown of SOAT1 decreases mammary tumor growth in vivo. Taken together, these findings suggest a largely undiscovered metabolic role for FGFR signaling in regulating cholesterol metabolism in breast cancer and present a therapeutic vulnerability that could be targeted in FGFR-driven cancers.

Indexed as

Breast NeoplasmsCholesterolReceptors, Fibroblast Growth FactorSterol O-AcyltransferaseAnimalsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessSignal TransductionCholesterolReceptors, Fibroblast Growth FactorSterol O-Acyltransferasesterol O-acyltransferase 1Cholesterol metabolismCholesterol storageFibroblast growth factorTriple-negative breast cancer

Identifiers

PMID40665359
PMCPMC12261779

What Socratic holds

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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 Socratic graph.