Evidence map›Paper›PMID 20847343›Full record

ArticleCancer research2010

High levels of Hsp90 cochaperone p23 promote tumor progression and poor prognosis in breast cancer by increasing lymph node metastases and drug resistance.

Natalie E Simpson, W Marcus Lambert, Renecia Watkins, Shah Giashuddin, S Joseph Huang, Ellinor Oxelmark, Rezina Arju, Tsivia Hochman, Judith D Goldberg, Robert J Schneider and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

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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

14 authors at 4 institutions in 2 countries.

Natalie E SimpsonDepartment of Pharmacology, and NYU Cancer Institute, NYU School of Medicine, New York, New York 10016, USA.
W Marcus Lambert
Renecia Watkins
Shah Giashuddin
S Joseph Huang
Ellinor Oxelmark
Rezina Arju
Tsivia Hochman
Judith D Goldberg
Robert J Schneider
Luiz Fernando Lima Reiz
Fernando Augusto Soares
Susan K Logan
Michael J Garabedian
Yale University · USCornell University · USNew York Hospital Queens · USHospital Sírio-Libanês · BR

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
ZOPOLRESTAT IN SUBJECTS W/ PERIPHERAL SYMMETRICAL DIABETIC POLYNEUROPATHYM01RR000096 · NCRR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NOVIK, YELENA · 1985 to 2008
$34.8M
NCI NIH HHS P30 CA016087NCI NIH HHS P30 CA16087NCRR NIH HHS M01 RR000096
6 · The paper itself

Abstract

p23 is a heat shock protein 90 (Hsp90) cochaperone located in both the cytoplasm and nucleus that stabilizes unliganded steroid receptors, controls the catalytic activity of certain kinases, regulates protein-DNA dynamics, and is upregulated in several cancers. We had previously shown that p23-overexpressing MCF-7 cells (MCF-7+p23) exhibit increased invasion without affecting the estrogen-dependent proliferative response, which suggests that p23 differentially regulates genes controlling processes linked to breast tumor metastasis. To gain a comprehensive view of the effects of p23 on estrogen receptor (ER)-dependent and -independent gene expression, we profiled mRNA expression from control versus MCF-7+p23 cells in the absence and presence of estrogen. A number of p23-sensitive target genes involved in metastasis and drug resistance were identified. Most striking is that many of these genes are also misregulated in invasive breast cancers, including PMP22, ABCC3, AGR2, Sox3, TM4SF1, and p8 (NUPR1). Upregulation of the ATP-dependent transporter ABCC3 by p23 conferred resistance to the chemotherapeutic agents etoposide and doxorubicin in MCF-7+p23 cells. MCF-7+p23 cells also displayed higher levels of activated Akt and an expanded phosphoproteome relative to control cells, suggesting that elevated p23 also enhances cytoplasmic signaling pathways. For breast cancer patients, tumor stage together with high cytoplasmic p23 expression more accurately predicted disease recurrence and mortality than did stage alone. High nuclear p23 was found to be associated with high cytoplasmic p23, therefore both may promote tumor progression and poor prognosis by increasing metastatic potential and drug resistance in breast cancer patients.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsBiomarkers, TumorBlotting, WesternBreast NeoplasmsCell ProliferationChromatin ImmunoprecipitationEstrogensFemaleGene Expression ProfilingHSP90 Heat-Shock ProteinsHumansImmunoenzyme TechniquesIntramolecular OxidoreductasesLymphatic MetastasisOligonucleotide Array Sequence AnalysisAntineoplastic AgentsBiomarkers, TumorEstrogensHSP90 Heat-Shock ProteinsIntramolecular OxidoreductasesProstaglandin-E SynthasesProto-Oncogene Proteins c-aktReceptors, EstrogenRNA, Messenger

Identifiers

PMID20847343
PMCPMC3007122
OpenAlexW2049250459

What OpenQuestion holds

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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.