Evidence map›Paper›PMID 22417809›Full record

ArticleBreast cancer research : BCR2012

Proteomic analysis of acquired tamoxifen resistance in MCF-7 cells reveals expression signatures associated with enhanced migration.

Changhua Zhou, Qiu Zhong, Lyndsay V Rhodes, Ian Townley, Melyssa R Bratton, Qiang Zhang, Elizabeth C Martin, Steven Elliott, Bridgette M Collins-Burow, Matthew E Burow and 1 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 113 citations in OpenAlex.

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  14. Characterization of Breast Cancer Aggressiveness by Cell Mechanics.International journal of molecular sciences · 2023
    Article
  15. Exploration of targeted anti-tumor therapy · 2022
    Review
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16 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 2 countries.

Changhua ZhouDepartment of Chemistry, Xavier University of Louisiana, 1 Drexel Drive, New Orleans, LA 70125, USA.
Qiu Zhong
Lyndsay V Rhodes
Ian Townley
Melyssa R Bratton
Qiang Zhang
Elizabeth C Martin
Steven Elliott
Bridgette M Collins-Burow
Matthew E Burow
Guangdi Wang
Tulane University · USXavier University of Louisiana · US

Funding

XAVIER'S RCMI CANCER RESEARCH PROGRAMG12RR026260 · NCRR · XAVIER UNIVERSITY OF LOUISIANA · PI D'AMOUR, GENE · 2009 to 2011
$7.0M
MEK5-Erk5 in breast cancer resistanceR01CA125806 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI BUROW, MATTHEW E. · 2010 to 2014
$1.5M
NCI NIH HHS CA125806NCI NIH HHS R01 CA125806NCRR NIH HHS 5G12RR026260-02NCRR NIH HHS G12 RR026260
6 · The paper itself

Abstract

introductionAcquired tamoxifen resistance involves complex signaling events that are not yet fully understood. Successful therapeutic intervention to delay the onset of hormone resistance depends critically on mechanistic elucidation of viable molecular targets associated with hormone resistance. This study was undertaken to investigate the global proteomic alterations in a tamoxifen resistant MCF-7 breast cancer cell line obtained by long term treatment of the wild type MCF-7 cell line with 4-hydroxytamoxifen (4-OH Tam).

methodsWe cultured MCF-7 cells with 4-OH Tam over a period of 12 months to obtain the resistant cell line. A gel-free, quantitative proteomic method was used to identify and quantify the proteome of the resistant cell line. Nano-flow high-performance liquid chromatography coupled to high resolution Fourier transform mass spectrometry was used to analyze fractionated peptide mixtures that were isobarically labeled from the resistant and control cell lysates. Real time quantitative PCR and Western blots were used to verify selected proteomic changes. Lentiviral vector transduction was used to generate MCF-7 cells stably expressing S100P. Online pathway analysis was performed to assess proteomic signatures in tamoxifen resistance. Survival analysis was done to evaluate clinical relevance of altered proteomic expressions.

resultsQuantitative proteomic analysis revealed a wide breadth of signaling events during transition to acquired tamoxifen resistance. A total of 629 proteins were found significantly changed with 364 up-regulated and 265 down-regulated. Collectively, these changes demonstrated the suppressed state of estrogen receptor (ER) and ER-regulated genes, activated survival signaling and increased migratory capacity of the resistant cell line. The protein S100P was found to play a critical role in conferring tamoxifen resistance and enhanced cell motility.

conclusionsOur data demonstrate that the adaptive changes in the proteome of tamoxifen resistant breast cancer cells are characterized by down-regulated ER signaling, activation of alternative survival pathways, and enhanced cell motility through regulation of the actin cytoskeleton dynamics. Evidence also emerged that S100P mediates acquired tamoxifen resistance and migration capacity.

Indexed as

Drug Resistance, NeoplasmActin CytoskeletonAntineoplastic Agents, HormonalBreast NeoplasmsCalcium-Binding ProteinsCell Line, TumorCell MovementDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansNeoplasm ProteinsProteomicsReceptors, EstrogenSignal TransductionTamoxifenAntineoplastic Agents, HormonalCalcium-Binding ProteinsNeoplasm ProteinsReceptors, EstrogenS100P protein, humanTamoxifen

Identifiers

PMID22417809
PMCPMC3446379
OpenAlexW2135688339

What OpenQuestion holds

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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.