Evidence map›Paper›PMID 15870198›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

STAT3- and DNA methyltransferase 1-mediated epigenetic silencing of SHP-1 tyrosine phosphatase tumor suppressor gene in malignant T lymphocytes.

Qian Zhang, Hong Y Wang, Michal Marzec, Puthiyaveettil N Raghunath, Tomohiko Nagasawa, Mariusz A Wasik

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
5.0field-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

149 citing papers in PubMed, 257 citations in OpenAlex.

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  12. Consideration of SHP-1 as a Molecular Target for Tumor Therapy.International journal of molecular sciences · 2023
    Review
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89 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

6 authors at 1 institution in 1 country.

Qian ZhangDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Hong Y Wang
Michal Marzec
Puthiyaveettil N Raghunath
Tomohiko Nagasawa
Mariusz A Wasik
University of Pennsylvania · US

Funding

Novel role of STAT3 in NPM/ALK-induced oncogenesisR01CA096856 · NCI · UNIVERSITY OF PENNSYLVANIA · PI WASIK, MARIUSZ A. · 2002 to 2013
$3.0M
Jak/STAT signaling in human T-cell lymphomasR01CA089194 · NCI · UNIVERSITY OF PENNSYLVANIA · PI WASIK, MARIUSZ A. · 2001 to 2010
$2.5M
Imaging of O6-Alkylguanine-DNA AlkyltransferaseR01CA093371 · NCI · DUKE UNIVERSITY · PI VAIDYANATHAN, GANESAN · 2002 to 2005
$1.2M
NCI NIH HHS P50-CA93371NCI NIH HHS R01 CA089194NCI NIH HHS R01 CA093371NCI NIH HHS R01 CA096856NCI NIH HHS R01-CA89194NCI NIH HHS R01-CA96856
6 · The paper itself

Abstract

Expression of SHP-1 phosphatase, a key negative regulator of cell signaling, is lost in T cell lymphomas and other malignancies due to DNA methylation of the SHP-1 promoter by a currently undefined mechanism. We demonstrate that malignant T cells express DNA methyltransferase (DNMT) 1 and that constantly activated signal transducer and activator of transcription (STAT) 3 is capable of binding in vitro to DNA oligonucleotides corresponding to four STAT3 SIE/GAS binding sites identified in the SHP-1 promoter. STAT3, DNMT1, and histone deacetylase 1 form complexes and bind to the SHP-1 promoter in vivo. Treatment with pharmacologic grade DNMT1 anti-sense oligonucleotides and STAT3 small-interfering RNA induces in the malignant T cells DNA demethylation and expression of SHP-1 gene. These data indicate that STAT3 may, in part, transform cells by inducing epigenetic silencing of SHP-1 in cooperation with DNMT1 and, apparently, histone deacetylase 1. Reversal of such gene silencing represents an attractive aim for novel anticancer therapies.

Indexed as

Gene SilencingBase SequenceBlotting, WesternCell Line, TumorChromatin ImmunoprecipitationCpG IslandsDNA-Binding ProteinsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Modification MethylasesDown-RegulationHistone Deacetylase 1Histone DeacetylasesHumansImmunohistochemistryDNA-Binding ProteinsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Modification MethylasesDNMT1 protein, humanHDAC1 protein, humanHistone Deacetylase 1Histone DeacetylasesIntracellular Signaling Peptides and ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPTPN6 protein, humanRNA, MessengerRNA, Small InterferingSTAT3 protein, humanSTAT3 Transcription FactorTrans-Activators

Identifiers

PMID15870198
PMCPMC1100783
OpenAlexW2029169197

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.