Evidence map›Paper›PMID 19351850›Full record

ArticleCancer research2009

Activation of the PI3 kinase pathway by retinoic acid mediates sodium/iodide symporter induction and iodide transport in MCF-7 breast cancer cells.

Emi Ohashi, Takahiko Kogai, Hiroyuki Kagechika, Gregory A Brent

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 46 citations in OpenAlex.

  1. 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
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  16. Retinoic acid signaling in axonal regeneration.Frontiers in molecular neuroscience · 2011
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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

4 authors at 3 institutions in 2 countries.

Emi OhashiMolecular Endocrinology Laboratory, VA Greater Los Angeles Healthcare System, Department of Medicine, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California 90073, USA.
Takahiko Kogai
Hiroyuki Kagechika
Gregory A Brent
University of California, Los Angeles · USTokyo Medical and Dental University · JPVA Greater Los Angeles Healthcare System · US

Funding

REGULATION OF THE SODIUM/IODIDE SYMPORTER IN BREASTR01CA089364 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRENT, GREGORY A · 2001 to 2011
$1.9M
NCI NIH HHS R01 CA089364
6 · The paper itself

Abstract

Iodide uptake in the thyroid and breast is mediated by the sodium/iodide symporter (NIS). NIS activation is used for radioiodide imaging and therapeutic ablation of thyroid carcinoma. NIS is expressed in >70% of breast cancers but at a level insufficient for radioiodine treatment. All-trans retinoic acid (tRA) induces NIS gene expression and functional iodide uptake in human breast cancer cell lines and mouse breast cancer models. tRA usually regulates gene expression by direct interaction of RA receptor (RAR) with a target gene, but it can also act through nongenomic pathways. We report a direct influence of tRA treatment on the phosphoinositide 3-kinase (PI3K) signal transduction pathway that mediates tRA-induced NIS expression in MCF-7 breast cancer cells. MCF-7 cells express all three RAR isoforms, alpha, beta, and gamma, and RXRalpha. We previously identified RARbeta and RXRalpha as important for NIS induction by tRA. Treatment with LY294002, the PI3K inhibitor, or p85alpha knockdown with siRNA abolished tRA-induced NIS expression. Immunoprecipitation experiments and glutathione S-transferase pull-down assay showed a direct interaction between RARbeta2, RXRalpha, and p85alpha. RA also induced rapid activation of Akt in MCF-7 cells. Treatment with an Akt inhibitor or Akt knockdown with siRNA reduced NIS expression. These findings indicate that RA induction of NIS in MCF-7 cells is mediated by rapid activation of the PI3K pathway and involves direct interaction with RAR and retinoid X receptor. Defining these mechanisms should lead to methods to further enhance NIS expression, as well as retinoid targets that influence growth and differentiation of breast cancer.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorChlorocebus aethiopsCOS CellsEnzyme ActivationHumansIodidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Retinoic AcidRetinoid X Receptor alphaSodium-Iodide SymportersSymportersTretinoinIodidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Retinoic Acidretinoic acid receptor betaRetinoid X Receptor alphaSodium-Iodide SymportersSymportersTretinoin

Identifiers

PMID19351850
PMCPMC2852426
OpenAlexW2009861669

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.