Evidence map›Paper›PMID 23183175›Full record

ArticleEndocrinology2013

Reactivation of the silenced thyroid hormone receptor β gene expression delays thyroid tumor progression.

Won Gu Kim, Xuguang Zhu, Dong Wook Kim, Lisa Zhang, Electron Kebebew, Sheue-Yann Cheng

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 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

6 authors at 2 institutions in 1 country.

Won Gu KimLaboratory of Molecular Biology, National Cancer Institute, 37 Convent Drive, Room 5128, Bethesda, MD 20892-4264, USA.
Xuguang Zhu
Dong Wook Kim
Lisa Zhang
Electron Kebebew
Sheue-Yann Cheng
National Cancer Institute · USCenter for Cancer Research · US

Funding

Preclinical Mouse Models of Thyroid CancerZIABC011191 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CHENG, SHEUE-YANN · 2009 to 2025
$13.8M
Thyroid Hormone Receptors in Health and DiseaseZIABC008752 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CHENG, SHEUE-YANN · 2009 to 2025
$12.9M
Genomic and genetic studies of endocrine cancersZIABC011275 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KEBEBEW, ELECTRON · 2010 to 2018
$8.2M
Intramural NIH HHS
6 · The paper itself

Abstract

That a knock-in mouse harboring a dominant-negative thyroid hormone receptor (TR)-β (Thrb) mutation develops metastatic thyroid cancer strongly suggests the involvement of TRβ in carcinogenesis. Epigenetic silencing of the THRB gene is common in human cancers. The aim of the present study was to determine how DNA methylation affected the expression of the THRB gene in differentiated thyroid cancer (DTC) and how reexpression of the THRB gene attenuated the cancer phenotypes. We used methylation-specific PCR to examine the expression and promoter methylation of the THRB gene in DTC tissues. Thyroid cancer cells with hypermethylated THRB were treated with the demethylating agents 5'-aza-2'-deoxycytidine (5'-aza-CdR) and zebularine to evaluate their impact on the cancer cell phenotypes. THRB mRNA expression in DTC was 90% lower than in normal controls, and this decrease was associated with a higher tumor/lymph node staging. The promoter methylation level of the THRB gene had a significant negative correlation with the expression level of the THRB gene. Treatment of FTC-236 cells with 5'-aza-CdR or zebularine induced reexpression of the THRB gene and inhibited cell proliferation and migration. FTC-236 cells stably expressing TRβ exhibited lower cell proliferation and migration through inhibition of β-catenin signaling pathways compared with FTC-236 without TRβ. 5'-Aza-CdR also led to suppression of tumor growth in an in vivo xenograft model using FTC-236 cells consistent with the cell-based studies. These finding indicate that TRβ is a tumor suppressor and could be tested as a potential therapeutic target.

Indexed as

AnimalsBlotting, WesternCell LineCell MovementCell ProliferationCytidineDNA MethylationHumansImmunohistochemistryMaleMiceMice, NudeReverse Transcriptase Polymerase Chain ReactionThyroid Hormone Receptors betaThyroid NeoplasmsXenograft Model Antitumor AssaysCytidinepyrimidin-2-one beta-ribofuranosideThyroid Hormone Receptors beta

Identifiers

PMID23183175
PMCPMC3529371
OpenAlexW1993797707

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.