Evidence map›Paper›PMID 28263968›Full record

ArticleOncogene2017

SND1 acts as a novel gene transcription activator recognizing the conserved Motif domains of Smad promoters, inducing TGFβ1 response and breast cancer metastasis.

L Yu, Y Di, L Xin, Y Ren, X Liu, X Sun, W Zhang, Z Yao, J Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% 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, 66 citations in OpenAlex.

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  11. Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    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

9 authors at 1 institution in 1 country.

L YuDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
Y DiDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
L XinDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
Y RenDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
X LiuDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
X SunDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
W ZhangDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
Z YaoDepartment of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
J YangDepartment of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As an AEG-1/MTDH/LYRIC-binding protein, Staphylococcal nuclease domain-containing 1 (SND1) is upregulated in numerous human cancers where it has been assigned multiple functional roles. In this study, we discovered that SND1 was upregulated in breast cancer tissues, particularly the tissues from patients with distant metastases. The underlying molecular mechanisms demonstrated a novel role of SND1 in regulating the activity of transforming growth factor β1 (TGFβ1) signaling pathway, which promotes metastasis in breast cancer. We illustrated that SND1 physically associated with and recruited the histone acetylase GCN5 to the promoter regions of Smad2/3/4, and consequently enhanced the gene transcriptional activation of Smad2/3/4, which are essential downstream regulators in the TGFβ1 pathway. An electrophoretic mobility shift assay experiment further verified that SND1 could recognize the conserved domains (motifs 1 and 2) in the promoter regions of the Smad genes. Glutathione S-transferase (GST) pulldown assays indicated that the tudor domain of SND1 was responsible for the recruitment of GCN5, which increased histone H3K9 acetylation. Consistent with these results, a loss-of-function of SND1 reduced the protein level of Smads and the phosphorylation of R-Smads, thereby attenuating the R-Smad/Co-Smad depended transcription and, as a result, inhibited TGFβ signaling activation.

Indexed as

AnimalsBase SequenceBreast NeoplasmsCell MovementConserved SequenceEndonucleasesFemaleGene ExpressionGene Expression Regulation, NeoplasticHEK293 CellsHumansKaplan-Meier EstimateLung NeoplasmsLymphatic MetastasisMCF-7 CellsMice, SCIDEndonucleasesNuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsSmad ProteinsSND1 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID28263968
OpenAlexW2592123165

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.