Evidence map›Paper›PMID 29109797›Full record

ArticleTheranostics2017

Notch3 Maintains Luminal Phenotype and Suppresses Tumorigenesis and Metastasis of Breast Cancer via Trans-Activating Estrogen Receptor-α.

Xiao-Wei Dou, Yuan-Ke Liang, Hao-Yu Lin, Xiao-Long Wei, Yong-Qu Zhang, Jing-Wen Bai, Chun-Fa Chen, Min Chen, Cai-Wen Du, Yao-Chen Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Theranostics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Modes of Notch signalling in development and disease.Nature reviews. Molecular cell biology · 2025
    Review
  5. Laminin α5: a key factor in tumor metastasis.Clinical & experimental metastasis · 2025
    Review
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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 3 countries.

Xiao-Wei DouThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Yuan-Ke LiangThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Hao-Yu LinThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Xiao-Long WeiThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Yong-Qu ZhangThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Jing-Wen BaiThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Chun-Fa ChenThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Min ChenChangJiang Scholar's Laboratory, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Cai-Wen DuDepartment of Breast Medical Oncology, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Yao-Chen LiThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Jie TianInstitute of Automation, Chinese Academy of Science, China.
Kwan ManDepartment of Surgery, Hong Kong University Li Ka-Tsing faculty of Medicine, Hong Kong, China.
Guo-Jun ZhangThe Breast Center, the Cancer Hospital of Shantou University Medical College (SUMC), China.
Shantou University · CNBreast Center · CHShandong Institute of Automation · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The luminal A phenotype is the most common breast cancer subtype and is characterized by estrogen receptor α expression (ERα). Identification of the key regulator that governs the luminal phenotype of breast cancer will clarify the pathogenic mechanism and provide novel therapeutic strategies for this subtype of cancer. ERα signaling pathway sustains the epithelial phenotype and inhibits the epithelial-mesenchymal transition (EMT) of breast cancer. In this study, we demonstrate that Notch3 positively associates with ERα in both breast cancer cell lines and human breast cancer tissues. We found that overexpression of Notch3 intra-cellular domain, a Notch3 active form (N3ICD), in ERα negative breast cancer cells re-activated ERα, while knock-down of Notch3 reduced ERα transcript and proteins, with alteration of down-stream genes, suggesting its ability to regulate ERα. Mechanistically, our results show that Notch3 specifically binds to the CSL binding element of the ERα promoter and activates ERα expression. Moreover, Notch3 suppressed EMT, while suppression of Notch3 promoted EMT in cellular assay. Overexpressing N3ICD in triple-negative breast cancer suppressed tumorigenesis and metastasis

Indexed as

Breast NeoplasmsCell Transformation, NeoplasticEpithelial-Mesenchymal TransitionErb-b2 Receptor Tyrosine KinasesEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansReceptor, Notch3Receptors, EstrogenErb-b2 Receptor Tyrosine KinasesESR1 protein, humanEstrogen Receptor alphaNOTCH3 protein, humanReceptor, Notch3Receptors, Estrogenbreast cancerepithelial-mesenchymal transitionestrogen receptor αluminal phenotype.Notch3

Identifiers

PMID29109797
PMCPMC5667424
OpenAlexW2757848583

What OpenQuestion holds

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Registered trials

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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.