Evidence map›Paper›PMID 22020934›Full record

ArticleThe Journal of biological chemistry2011

Progesterone receptor inhibits proliferation of human breast cancer cells via induction of MAPK phosphatase 1 (MKP-1/DUSP1).

Chien-Cheng Chen, Daniel B Hardy, Carole R Mendelson

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

33 citing papers in PubMed, 68 citations in OpenAlex.

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  6. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    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

3 authors at 2 institutions in 2 countries.

Chien-Cheng ChenDepartments of Biochemistry and Obstetrics & Gynecology, North Texas March of Dimes Birth Defects Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Daniel B Hardy
Carole R Mendelson
The University of Texas Southwestern Medical Center · USWestern University · CA

Funding

CELLULAR MECHANISMS IN THE INDUCTION OF AROMATASER01DK031206 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MENDELSON, CAROLE R · 1985 to 2015
$5.5M
Cellular Mechanisms in the Induction of AromataseR56DK031206 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MENDELSON, CAROLE R · 2010 to 2010
$238k
NIDDK NIH HHS 2-R56-DK031206NIDDK NIH HHS 5-R01-DK031206NIDDK NIH HHS R01 DK031206NIDDK NIH HHS R56 DK031206
6 · The paper itself

Abstract

The roles of progesterone (P(4)) and of progesterone receptor (PR) in development and pathogenesis of breast cancer remain unclear. In this study, we observed that treatment of T47D breast cancer cells with progestin antagonized effects of fetal bovine serum (FBS) to stimulate cell proliferation, whereas siRNA-mediated knockdown of endogenous PR abrogated progestin-mediated anti-proliferative effects. To begin to define mechanisms for the anti-proliferative action of P(4)/PR, we considered the role of MAPK phosphatase 1 (MKP-1/DUSP1), which catalyzes dephosphorylation and inactivation of MAPKs. Progestin treatment of T47D cells rapidly induced MKP-1 expression in a PR-dependent manner. Importantly, P(4) induction of MKP-1 was associated with reduced levels of phosphorylated ERK1/2, whereas siRNA knockdown of MKP-1 blocked progestin-mediated ERK1/2 dephosphorylation and repression of FBS-induced cell proliferation. The importance of PR in MKP-1 expression was supported by findings that MKP-1 and PR mRNA levels were significantly correlated in 30 human breast cancer cell lines. By contrast, no correlation was observed with the glucocorticoid receptor, a known regulator of MKP-1 in other cell types. ChIP and luciferase reporter assay findings suggest that PR acts in a ligand-dependent manner through binding to two progesterone response elements downstream of the MKP-1 transcription start site to up-regulate MKP-1 promoter activity. PR also interacts with two Sp1 sites just downstream of the transcription start site to increase MKP-1 expression. Collectively, these findings suggest that MKP-1 is a critical mediator of anti-proliferative and anti-inflammatory actions of PR in the breast.

Indexed as

Breast NeoplasmsCell LineCell Line, TumorCell ProliferationChromatin ImmunoprecipitationDual Specificity Phosphatase 1Gene Expression Regulation, NeoplasticHumansImmunoblottingMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProgesteronePromegestoneReal-Time Polymerase Chain ReactionReceptors, ProgesteroneDual Specificity Phosphatase 1Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3ProgesteronePromegestoneReceptors, Progesterone

Identifiers

PMID22020934
PMCPMC3234857
OpenAlexW2005028301

What OpenQuestion holds

Textmetadata
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.