Evidence map›Paper›PMID 26219409›Full record

ArticleScientific reports2015

Identification of Estrogen Response Element in Aquaporin-3 Gene that Mediates Estrogen-induced Cell Migration and Invasion in Estrogen Receptor-positive Breast Cancer.

Yi-Ting Huang, Jun Zhou, Shuai Shi, Hai-Yan Xu, Fan Qu, Dan Zhang, Yi-Ding Chen, Jing Yang, He-Feng Huang, Jian-Zhong Sheng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Article
  16. Aquaporin-mediated dysregulation of cell migration in disease states.Cellular and molecular life sciences : CMLS · 2023
    Review
  17. Methods for studying mammalian aquaporin biology.Biology methods & protocols · 2023
    Review
  18. Clinical value and molecular mechanism of AQGPs in different tumors.Medical oncology (Northwood, London, England) · 2022
    Review
  19. Article
  20. 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

10 authors at 4 institutions in 1 country.

Yi-Ting Huang1] Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China [2] The Key Laboratory of Reproductive Genetics, Ministry of Education (Zhejiang University), Hangzhou, Zhejiang, China.
Jun ZhouWomen's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Shuai ShiDepartment of Medical Reproductive Centre, People's Hospital of Jinhuan City, Jinhua, Zhejiang, China.
Hai-Yan XuThe Key Laboratory of Reproductive Genetics, Ministry of Education (Zhejiang University), Hangzhou, Zhejiang, China.
Fan QuWomen's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Dan ZhangWomen's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Yi-Ding ChenThe Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Jing YangThe Key Laboratory of Reproductive Genetics, Ministry of Education (Zhejiang University), Hangzhou, Zhejiang, China.
He-Feng Huang1] The Key Laboratory of Reproductive Genetics, Ministry of Education (Zhejiang University), Hangzhou, Zhejiang, China [2] International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jian-Zhong Sheng1] Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China [2] The Key Laboratory of Reproductive Genetics, Ministry of Education (Zhejiang University), Hangzhou, Zhejiang, China.
Zhejiang University · CNWomen's Hospital, School of Medicine, Zhejiang University · CNSecond Affiliated Hospital of Zhejiang University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests that aquaporins (AQPs) may facilitate tumor development. The molecular pathways connecting the pathological functions of AQPs are unclear and need to be better defined. This study aimed to investigate whether AQP3, one of the AQPs expressed highly in breast cancer, had any clinical implication in estrogen-receptor (ER) positive breast cancer, and explore the regulatory mechanisms of AQP3 in estrogen-related breast cancer progression. Here we show that AQP3 is an important enforcer of migration and invasion in breast cancer. We, for the first time, reported that ER-positive breast cancer tissues obtained from premenopausal patients had higher AQP3 expression when compared to those obtained from postmenopausal patients. Estrogen directly upregulates AQP3 by activating ERE in the promoter of the AQP3 gene. The upregulation of AQP3 can influence the expression of molecules related to epithelial-mesenchymal transition and the reorganization of actin-cytoskeleton, resulting in enhancement of cell migration and invasion in ER-positive breast cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticResponse ElementsActinsAdultAgedAquaporin 3Breast NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionEstrogensFemaleGene ExpressionGene Knockdown TechniquesHumansImmunohistochemistryActinsAquaporin 3EstrogensReceptors, Estrogen

Identifiers

PMID26219409
PMCPMC4518221
OpenAlexW2408372990

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.