Evidence map›Paper›PMID 20664923›Full record

ArticleInternational journal of oncology2010

Regulation of ERalpha-mediated transcription of Bcl-2 by PI3K-AKT crosstalk: implications for breast cancer cell survival.

Melyssa R Bratton, Bich N Duong, Steven Elliott, Christopher B Weldon, Barbara S Beckman, John A McLachlan, Matthew E Burow

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.0field-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

30 citing papers in PubMed, 66 citations in OpenAlex.

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  13. The effects of interleukin-2 on immune response regulation.Mathematical medicine and biology : a journal of the IMA · 2018
    Article
  14. Article
  15. 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

7 authors at 1 institution in 1 country.

Melyssa R BrattonTulane University School of Medicine, Department of Pharmacology, 1430 Tulane Ave., New Orleans, LA 70112, USA.
Bich N Duong
Steven Elliott
Christopher B Weldon
Barbara S Beckman
John A McLachlan
Matthew E Burow
Tulane University · US

Funding

P13K/AKT crosstalk with ER-signaling and cell survivalR01DK059389 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI BUROW, MATTHEW E. · 2003 to 2008
$1.8M
RESEARCH TRAINING IN SURGICAL ONCOLOGY (T32)T32CA065436 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI JAFFE, BERNARD M · 1997 to 2001
$62k
NCI NIH HHS 1 T32 CA65436-01A3NCI NIH HHS T32 CA065436NIDDK NIH HHS 5R01DK059389-06NIDDK NIH HHS R01 DK059389PHS HHS R06/CCR419466-02
6 · The paper itself

Abstract

Both estrogen, through the estrogen receptor (ER), and growth factors, through the phosphatidylinositol-3-kinase (PI3K)-AKT pathway, have been shown to independently promote cell survival. Here, we investigated the role of ER/PI3K-AKT crosstalk in the regulation of cell survival in MCF-7 breast carcinoma cells. The ER inhibitor ICI 182,780 was used to determine the requirement of the ER for estrogen in the suppression of tumor necrosis factor-alpha (TNFalpha) induced apoptosis. Gene reporter assays and Western blot analyses were used to determine the involvement of the pro-survival factor Bcl-2 and the coactivator GRIP1 in this survival crosstalk. We demonstrated that an intact ER signaling pathway was required for estrogen to suppress apoptosis induced by TNFalpha. Our gene reporter assays revealed that ERalpha, not ERbeta, was targeted by AKT, resulting in transcriptional potentiation of the full-length Bcl-2 promoter, ultimately leading to increased Bcl-2 protein levels. AKT targeted both activation function (AF) domains of the ERalpha for maximal induction of Bcl-2 reporter activity, although the AF-II domain was predominately targeted. In addition, AKT also caused an upregulation of GRIP1 protein levels. Finally, AKT and GRIP1 cooperated to increase Bcl-2 protein expression to a greater level than either factor alone. Collectively, our study suggests a role for ER/PI3K-AKT crosstalk in cell survival and documents the ability of AKT to regulate Bcl-2 expression via differential activation of ERalpha and ERbeta as well as regulation of GRIP1.

Indexed as

Breast NeoplasmsCarrier ProteinsCell Line, TumorCell SurvivalEstrogen Receptor alphaEstrogensFemaleGene Expression Regulation, NeoplasticHumansNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Signal TransductionSurvival AnalysisTranscription, GeneticCarrier ProteinsEstrogen Receptor alphaEstrogensGRIP1 protein, humanNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Tumor Necrosis Factor-alpha

Identifiers

PMID20664923
PMCPMC3613138
OpenAlexW2151282923

What OpenQuestion holds

Textmetadata
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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.