Evidence map›Paper›PMID 20374646›Full record

ArticleBMC cancer2010

STAMP alters the growth of transformed and ovarian cancer cells.

Yuanzheng He, John A Blackford, Elise C Kohn, S Stoney Simons

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Novel somatic alterations underlie Chinese papillary thyroid carcinoma.Cancer biomarkers : section A of Disease markers · 2020
    Article
  2. Article
  3. Article
  4. Article
  5. Glucocorticoid receptor cofactors as therapeutic targets.Current opinion in pharmacology · 2010
    Review
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

4 authors at 3 institutions in 1 country.

Yuanzheng HeSteroid Hormones Section, Clinical Endocrinology Branch, NIDDK, National Institutes of Health, Bethesda, MD 20892-1772, USA.
John A Blackford
Elise C Kohn
S Stoney Simons
National Institutes of Health · USNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health Clinical Center · US

Funding

Modulation of parameters of glucocorticoid receptor-mediated gene repressionZIADK047040 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONS, S STONEY · 2009 to 2015
$2.0M
Signal Transduction Therapy--Basic ScienceZIASC009163 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI KOHN, ELISE C. · 2009 to 2013
$1.4M
Mechanism of action of STAMP - a new comodulator of glucocorticoid receptorsZIADK047039 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONS, S S · 2009 to 2013
$984k
Intramural NIH HHS
6 · The paper itself

Abstract

backgroundSteroid receptors play major roles in the development, differentiation, and homeostasis of normal and malignant tissue. STAMP is a novel coregulator that not only enhances the ability of p160 coactivator family members TIF2 and SRC-1 to increase gene induction by many of the classical steroid receptors but also modulates the potency (or EC50) of agonists and the partial agonist activity of antisteroids. These modulatory activities of STAMP are not limited to gene induction but are also observed for receptor-mediated gene repression. However, a physiological role for STAMP remains unclear.

methodsThe growth rate of HEK293 cells stably transfected with STAMP plasmid and overexpressing STAMP protein is found to be decreased. We therefore asked whether different STAMP levels might also contribute to the abnormal growth rates of cancer cells. Panels of different stage human cancers were screened for altered levels of STAMP mRNA. Those cancers with the greatest apparent changes in STAMP mRNA were pursued in cultured cancer cell lines.

resultsHigher levels of STAMP are shown to have the physiologically relevant function of reducing the growth of HEK293 cells but, unexpectedly, in a steroid-independent manner. STAMP expression was examined in eight human cancer panels. More extensive studies of ovarian cancers suggested the presence of higher levels of STAMP mRNA. Lowering STAMP mRNA levels with siRNAs alters the proliferation of several ovarian cancer tissue culture lines in a cell line-specific manner. This cell line-specific effect of STAMP is not unique and is also seen for the conventional effects of STAMP on glucocorticoid receptor-regulated gene transactivation.

conclusionsThis study indicates that a physiological function of STAMP in several settings is to modify cell growth rates in a manner that can be independent of steroid hormones. Studies with eleven tissue culture cell lines of ovarian cancer revealed a cell line-dependent effect of reduced STAMP mRNA on cell growth rates. This cell-line dependency is also seen for STAMP effects on glucocorticoid receptor-mediated transactivation. These preliminary findings suggest that further studies of STAMP in ovarian cancer may yield insight into ovarian cancer proliferation and may be useful in the development of biomarker panels.

Indexed as

Carrier ProteinsCell Growth ProcessesCell LineCell Line, TumorCell Transformation, NeoplasticFemaleHumansKidneyOvarian NeoplasmsRNA, MessengerRNA, Small InterferingTranscriptional ActivationTransfectionCarrier ProteinsRNA, MessengerRNA, Small InterferingTTLL5 protein, human

Identifiers

PMID20374646
PMCPMC2858746
OpenAlexW1988261960

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.