Evidence map›Paper›PMID 28098816›Full record

ArticleInternational journal of molecular sciences2017

Estrogen Enhances the Expression of the Multidrug Transporter Gene ABCG2-Increasing Drug Resistance of Breast Cancer Cells through Estrogen Receptors.

Fung-Wei Chang, Hueng-Chuen Fan, Jui-Ming Liu, Tai-Ping Fan, Jin Jing, Chia-Ling Yang, Ren-Jun Hsu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 62 citations in OpenAlex.

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  16. Multidrug efflux transporter ABCG2: expression and regulation.Cellular and molecular life sciences : CMLS · 2021
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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

7 authors at 4 institutions in 2 countries.

Fung-Wei ChangDepartment of Obstetrics & Gynecology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan. doc30666@gmail.com.
Hueng-Chuen FanDepartment of Pediatrics, Tungs' Taichung MetroHarbor Hospital, Taichung 435, Taiwan. fanhuengchuen@yahoo.com.tw.
Jui-Ming LiuDivision of Urology, Department of Surgery, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan 333, Taiwan. mento1218@gmail.com.
Tai-Ping FanDepartment of Pharmacology, University of Cambridge, Cambridge CB23 8AQ, UK. tpf1000@cam.ac.uk.
Jin JingDepartment of Pharmacology, University of Cambridge, Cambridge CB23 8AQ, UK. jinjing1207@hotmail.com.
Chia-Ling YangDepartment of Pharmacology, University of Cambridge, Cambridge CB23 8AQ, UK. cly2375@gmail.com.
Ren-Jun HsuGraduate Institute of Life Sciences, National Defense Medical Center, Taipei 114, Taiwan. hsurnai@gmail.com.
University of Cambridge · GBTri-Service General Hospital · TWMinistry of Health and Welfare · TWTungs' Taichung MetroHarbor Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultidrug resistance is a major obstacle in the successful therapy of breast cancer. Studies have proved that this kind of drug resistance happens in both human cancers and cultured cancer cell lines. Understanding the molecular mechanisms of drug resistance is important for the reasonable design and use of new treatment strategies to effectively confront cancers.

resultsIn our study, ATP-binding cassette sub-family G member 2 (ABCG2), adenosine triphosphate (ATP) synthase and cytochrome c oxidase subunit VIc (COX6C) were over-expressed more in the MCF-7/MX cell line than in the normal MCF7 cell line. Therefore, we believe that these three genes increase the tolerance of MCF7 to mitoxantrone (MX). The data showed that the high expression of COX6C made MCF-7/MX have more stable on mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) expression than normal MCF7 cells under hypoxic conditions. The accumulation of MX was greater in the ATP-depleted treatment MCF7/MX cells than in normal MCF7/MX cells. Furthermore, E2 increased the tolerance of MCF7 cells to MX through inducing the expression of ABCG2. However, E2 could not increase the expression of ABCG2 after the inhibition of estrogen receptor α (ERα) in MCF7 cells. According to the above data, under the E2 treatment, MDA-MB231, which lacks ER, had a higher sensitivity to MX than MCF7 cells.

conclusionsE2 induced the expression of ABCG2 through ERα and the over-expressed ABCG2 made MCF7 more tolerant to MX. Moreover, the over-expressed ATP synthase and COX6c affected mitochondrial genes and function causing the over-expressed ABCG2 cells pumped out MX in a concentration gradient from the cell matrix. Finally lead to chemoresistance.

Indexed as

Adenosine TriphosphateATP Binding Cassette Transporter, Subfamily G, Member 2Breast NeoplasmsCell DeathCell HypoxiaDrug Resistance, NeoplasmEstrogensFemaleGene Expression Regulation, NeoplasticGenes, MitochondrialHumansMCF-7 CellsModels, BiologicalOligonucleotide Array Sequence AnalysisReactive Oxygen SpeciesReceptors, EstrogenAdenosine TriphosphateATP Binding Cassette Transporter, Subfamily G, Member 2EstrogensReactive Oxygen SpeciesReceptors, EstrogenATP-binding cassette sub-family G member 2 (ABCG2)breast cancerestrogen, estrogen receptor α (ERα)mitoxantrone (MX)

Identifiers

PMID28098816
PMCPMC5297796
OpenAlexW2573688693

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.