Evidence map›Paper›PMID 24481325›Full record

ArticleEndocrine-related cancer2014

GPER-mediated proliferation and estradiol production in breast cancer-associated fibroblasts.

Haojun Luo, Guanglun Yang, Tenghua Yu, Shujuan Luo, Chengyi Wu, Yan Sun, Manran Liu, Gang Tu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrine-related cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
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  4. Targeting CAF-specific metabolic pathways in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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  16. Characterization of Breast Cancer Aggressiveness by Cell Mechanics.International journal of molecular sciences · 2023
    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

8 authors at 3 institutions in 1 country.

Haojun LuoDepartment of Breast and Thyroid Surgery, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China Department of Endocrine and Breast Surgery, the First Affiliated Hospital of Chongqing Medical University, No. 1 You-Yi Road, Yu-zhong District, Chongqing 400016, China Department of Gynecology and Obstetrics, Chongqing Health Center for Women and Children, Chongqing 400010, China Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, No. 1 Yi-Xue-Yuan Road, Yu-zhong District, Chongqing 400016, China.
Guanglun Yang
Tenghua Yu
Shujuan Luo
Chengyi Wu
Yan Sun
Manran Liu
Gang Tu
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) are crucial co-mediators of breast cancer progression. Estrogen is the predominant driving force in the cyclic regulation of the mammary extracellular matrix, thus potentially affecting the tumor-associated stroma. Recently, a third estrogen receptor, estrogen (G-protein-coupled) receptor (GPER), has been reported to be expressed in breast CAFs. In this study, GPER was detected by immunohistochemical analysis in stromal fibroblasts of 41.8% (59/141) of the primary breast cancer samples. GPER expression in CAFs isolated from primary breast cancer tissues was confirmed by immunostaining and RT-PCR analyses. Tamoxifen (TAM) in addition to 17β-estradiol (E₂) and the GPER agonist G1 activated GPER, resulting in transient increases in cell index, intracellular calcium, and ERK1/2 phosphorylation. Furthermore, TAM, E₂, and G1 promoted CAF proliferation and cell-cycle progression, both of which were blocked by GPER interference, the selective GPER antagonist G15, the epidermal growth factor receptor (EGFR) inhibitor AG1478, and the ERK1/2 inhibitor U0126. Importantly, TAM as well as G1 increased E₂ production in breast CAFs via GPER/EGFR/ERK signaling when the substrate of E₂, testosterone, was added to the medium. GPER-induced aromatase upregulation was probably responsible for this phenomenon, as TAM- and G1-induced CYP19A1 gene expression was reduced by GPER knockdown and G15, AG1478, and U0126 administration. Accordingly, GPER-mediated CAF-dependent estrogenic effects on the tumor-associated stroma are conceivable, and CAF is likely to contribute to breast cancer progression, especially TAM resistance, via a positive feedback loop involving GPER/EGFR/ERK signaling and E₂ production.

Indexed as

Cell ProliferationBreast NeoplasmsCell CycleCells, CulturedCyclopentanesEstradiolFemaleFibroblastsHumansQuinolinesReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifen1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanoneCyclopentanesEstradiolGPER1 protein, humanQuinolinesReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifenbreast cancerCAFGPERtamoxifen resistance

Identifiers

PMID24481325
PMCPMC3959763
OpenAlexW2161118254

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.