Evidence map›Paper›PMID 24160469›Full record

ArticleMolecular cancer2013

Small molecule antagonist of the bone morphogenetic protein type I receptors suppresses growth and expression of Id1 and Id3 in lung cancer cells expressing Oct4 or nestin.

Elaine Langenfeld, Malik Deen, Emmanuel Zachariah, John Langenfeld

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

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  9. Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy.International journal of medical sciences · 2020
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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 2 institutions in 1 country.

Elaine Langenfeld
Malik Deen
Emmanuel Zachariah
John LangenfeldDivision of Thoracic Surgery, Rutgers-Robert Wood Johnson Medical School, One Robert Wood Johnson Place, P,O, Box 19, New Brunswick, NJ 08903-0019, USA. langenje@rwjms.rutgers.edu.
Johnson University · USRutgers, The State University of New Jersey · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBone morphogenetic proteins (BMP) are embryonic morphogens that are aberrantly expressed in lung cancer. BMPs mediate cell fate decisions and self-renewal of stem cells, through transcription regulation of inhibitor of differentiation protein/DNA binding proteins (Id1-3). Inhibition of BMP signaling decreases growth and induces cell death of lung cancer cells lines by downregulating the expression of Id proteins. It is not known whether the BMP signaling cascade regulates growth and the expression of Id proteins of lung cancer cells expressing the stem cell markers Oct4 and/or nestin.

methodsLung cancer cells expressing Oct4 or nestin were isolated from lung cancer cell lines by stably transfecting the Oct4 promoter or nestin promoter expression vectors that induce expression of the green fluorescent protein reporter.

resultsOur studies suggest that lung cancer cells expressing Oct4 or nestin are different cell populations. Microarray and quantitative RT-PCR demonstrated that the expression of specific stem cell markers were different between isolated Oct4 and nestin cells. Both the Oct4 and nestin populations were more tumorigenic than controls but histologically they were quite different. The isolated Oct4 and nestin cells also responded differently to inhibition of BMP signaling. Blockade of BMP signaling with the BMP receptor antagonist DMH2 caused significant growth inhibition of both the Oct4 and nestin cell populations but only increased cell death in the nestin population. DMH2 also induced the expression of nestin in the Oct4 population but not in the nestin cells. We also show that BMP signaling is an important regulator of Id1 and Id3 in both the Oct4 and nestin cell populations. Furthermore, we show that NeuN is frequently expressed in NSCLC and provide evidence suggesting that Oct4 cells give rise to cancer cells expressing nestin and/or NeuN.

conclusionThese studies show that although biologically different, BMP signaling is growth promoting in cancer cells expressing Oct4 or nestin. Inhibition of BMP signaling decreases expression of Id proteins and suppresses growth of cancer cells expressing Oct4 or Nestin. Small molecule antagonists of the BMP type I receptors represent potential novel drugs to target the population of cancer cells expressing stem cell markers.

Indexed as

AnimalsAntigens, NuclearAntineoplastic AgentsBiomarkers, TumorBone Morphogenetic Protein Receptors, Type ICarcinoma, Non-Small-Cell LungCell Line, TumorHumansInhibitor of Differentiation Protein 1Inhibitor of Differentiation ProteinsLung NeoplasmsMiceMice, NudeNeoplasm ProteinsNeoplasm TransplantationNeoplastic Stem CellsAntigens, NuclearAntineoplastic AgentsBiomarkers, TumorBone Morphogenetic Protein Receptors, Type IID1 protein, humanID3 protein, humanInhibitor of Differentiation Protein 1Inhibitor of Differentiation ProteinsNeoplasm ProteinsNerve Tissue ProteinsNES protein, humanNestinneuronal nuclear antigen NeuN, humanOctamer Transcription Factor-3POU5F1 protein, human

Identifiers

PMID24160469
PMCPMC4176118
OpenAlexW2150262642

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.