Evidence map›Paper›PMID 30535436›Full record

ArticleMolecular medicine reports2019

Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells.

Shuang Liu, Huan Hou, Panpan Zhang, Yifan Wu, Xuanhong He, Hua Li, Nianlong Yan

Abstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. The Interplay Between TGF-β Signaling and Cell Metabolism.Frontiers in cell and developmental biology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Observational
  12. Article
  13. Article
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

7 authors.

Shuang Liu *Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Huan Hou *Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Panpan Zhang *Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Yifan WuDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Xuanhong HeDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Hua LiDepartment of Biochemistry and Molecular Biology, Centre of Experimental Medicine, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Nianlong YanDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the most common cancer in women and a leading cause of cancer‑associated mortalities in the world. Epithelial‑to‑mesenchymal transition (EMT) serves an important role in the process of metastasis and invasive ability in cancer cells, and transforming growth factor β1 (TGF‑β1) have been investigated for promoting EMT. However, in the present study, the role of the sphingomyelin synthase 1 (SMS1) in TGF‑β1‑induced EMT development was investigated. Firstly, bioinformatics analysis demonstrated that the overexpression of SMS1 negatively regulated the TGFβ receptor I (TβRI) level of expression. Subsequently, the expression of SMS1 was decreased, whereas, SMS2 had no significant difference when MDA‑MB‑231 cells were treated by TGF‑β1 for 72 h. Furthermore, the present study constructed an overexpression cells model of SMS1 and these cells were treated by TGF‑β1. These results demonstrated that overexpression of SMS1 inhibited TGF‑β1‑induced EMT and the migration and invasion of MDA‑MB‑231 cells, increasing the expression of E‑cadherin while decreasing the expression of vimentin. Furthermore, the present study further confirmed that SMS1 overexpression could decrease TβRI expression levels and blocked smad family member 2 phosphorylation. Overall, the present results suggested that SMS1 could inhibit EMT and the migration and invasion of MDA‑MB‑231 cells via TGF‑β/Smad signaling pathway.

Indexed as

CadherinsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene ExpressionHumansMCF-7 CellsMembrane ProteinsNeoplasm InvasivenessNerve Tissue ProteinsPhosphorylationSignal TransductionSmad ProteinsTransferases (Other Substituted Phosphate Groups)Transforming Growth Factor beta1VimentinCadherinsMembrane ProteinsNerve Tissue ProteinsSGMS1 protein, humanSmad ProteinsTGFB1 protein, humanTransferases (Other Substituted Phosphate Groups)Transforming Growth Factor beta1Vimentinepithelial-to-mesenchymal transitionMDA-MB-231 cellssphingomyelin synthase 1transforming growth factor β1

Identifiers

PMID30535436
PMCPMC6323219

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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.