Evidence map›Paper›PMID 26354229›Full record

ArticleNature communications2015

Epigenetic regulation of Smad2 and Smad3 by profilin-2 promotes lung cancer growth and metastasis.

Yun-Neng Tang, Wei-Qiao Ding, Xiao-Jie Guo, Xin-Wang Yuan, Dong-Mei Wang, Jian-Guo Song

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 120 citations in OpenAlex.

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18 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 3 institutions in 1 country.

Yun-Neng TangState Key Laboratory of Cell Biology, Innovation Center for Cell Signalling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Wei-Qiao DingState Key Laboratory of Cell Biology, Innovation Center for Cell Signalling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Xiao-Jie GuoState Key Laboratory of Cell Biology, Innovation Center for Cell Signalling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Xin-Wang YuanState Key Laboratory of Cell Biology, Innovation Center for Cell Signalling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Dong-Mei WangState Key Laboratory of Cell Biology, Innovation Center for Cell Signalling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Jian-Guo SongState Key Laboratory of Cell Biology, Innovation Center for Cell Signalling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Chinese Academy of Sciences · CNCenter for Excellence in Molecular Cell Science · CNShanghai Institutes for Biological Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered transforming growth factor-β (TGF-β) signalling has been implicated in tumour development and progression. However, the molecular mechanism behind this alteration is poorly understood. Here we show that profilin-2 (Pfn2) increases Smad2 and Smad3 expression via an epigenetic mechanism, and that profilin-2 and Smad expression correlate with an unfavourable prognosis of lung cancer patients. Profilin-2 overexpression promotes, whereas profilin-2 knockdown drastically reduces, lung cancer growth and metastasis. We show that profilin-2 suppresses the recruitment of HDAC1 to Smad2 and Smad3 promoters by preventing nuclear translocation of HDAC1 through protein-protein interaction at the C terminus of both proteins, leading to the transcriptional activation of Smad2 and Smad3. Increased Smad2 and Smad3 expression enhances TGF-β1-induced EMT and production of the angiogenic factors VEGF and CTGF. These findings reveal a new regulatory mechanism of TGF-β1/Smad signalling, and suggest a potential molecular target for the development of anticancer drugs.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticAnimalsCell Line, TumorChromatin ImmunoprecipitationConnective Tissue Growth FactorEpigenesis, GeneticFlow CytometryFluorescent Antibody TechniqueHEK293 CellsHistone Deacetylase 1HumansImmunohistochemistryImmunoprecipitationLung NeoplasmsMiceCCN2 protein, humanConnective Tissue Growth FactorHDAC1 protein, humanHistone Deacetylase 1PFN2 protein, humanProfilinsSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1Vascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID26354229
OpenAlexW2201057556

What OpenQuestion holds

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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.