Evidence map›Paper›PMID 22359623›Full record

ArticlePloS one2012

Induction of sodium/iodide symporter (NIS) expression and radioiodine uptake in non-thyroid cancer cells.

Zhi Liu, Mingzhao Xing

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  5. Review
  6. Unusual Uptake of [Molecular imaging and radionuclide therapy · 2022
    Article
  7. Article
  8. Therapeutic targeting of FOS in mutantProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019
    Article
  13. Article
  14. Article
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  17. 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

2 authors at 1 institution in 1 country.

Zhi LiuLaboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, School of Medicine, Johns Hopkins University, Baltimore, Maryland, United States of America.
Mingzhao Xing
Johns Hopkins University · US

Funding

Molecular Events in the PI3K/Akt Pathway in Thyroid CancerR01CA134225 · NCI · JOHNS HOPKINS UNIVERSITY · PI XING, MICHAEL MINGZHAO · 2009 to 2013
$1.6M
NCI NIH HHS R01 CA134225NCI NIH HHS R01 CA134225
6 · The paper itself

Abstract

backgroundThis study was designed to explore the therapeutic potential of suppressing MAP kinase and PI3K/Akt pathways and histone deacetylase (HDAC) to induce the expression of sodium/iodide symporter (NIS) and radioiodine uptake in non-thyroid cancer cells.

methodsWe tested the effects of the MEK inhibitor RDEA119, the Akt inhibitor perifosine, and the HDAC inhibitor SAHA on NIS expression in thirteen human cancer cell lines derived from melanoma, hepatic carcinoma, gastric carcinoma, colon carcinoma, breast carcinoma, and brain cancers. We also examined radioiodine uptake and histone acetylation at the NIS promoter in selected cells.

resultsOverall, the three inhibitors could induce NIS expression, to various extents, in melanoma and all the epithelial carcinoma-derived cells but not in brain cancer-derived cells. SAHA was most effective and its effect could be significantly enhanced by RDEA119 and perifosine. The expression of NIS, at both mRNA and protein levels, was most robust in the melanoma cell M14, hepatic carcinoma cell HepG2, and the gastric carcinoma cell MKN-7 cell. Radioiodine uptake was correspondingly induced, accompanied by robust increase in histone acetylation at the NIS promoter, in these cells when treated with the three inhibitors.

conclusionsThis is the first demonstration that simultaneously suppressing the MAP kinase and PI3K/Akt pathways and HDAC could induce robust NIS expression and radioiodine uptake in certain non-thyroid human cancer cells, providing novel therapeutic implications for adjunct radioiodine treatment of these cancers.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsCell Line, TumorDiphenylamineHistone Deacetylase InhibitorsHumansHydroxamic AcidsIodine RadioisotopesMitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesPhosphorylcholineSignal TransductionSodium-Iodide SymportersSulfonamidesSymportersTranscriptional ActivationVorinostatDiphenylamineHistone Deacetylase InhibitorsHydroxamic AcidsIodine RadioisotopesMitogen-Activated Protein Kinase KinasesN-(3,4-difluoro-2-(2-fluoro-4-iodophenylamino)-6-methoxyphenyl)-1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonamideperifosinePhosphatidylinositol 3-KinasesPhosphorylcholineSodium-Iodide SymportersSulfonamidesSymportersVorinostat

Identifiers

PMID22359623
PMCPMC3281006
OpenAlexW2012438105

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.