Evidence map›Paper›PMID 29795373›Full record

ArticleCell death & disease2018

Gamma synuclein is a novel Twist1 target that promotes TGF-β-induced cancer cell migration and invasion.

Ting Shao, Peiying Song, Hui Hua, Hongying Zhang, Xiangmin Sun, Qingbin Kong, Jiao Wang, Ting Luo, Yangfu Jiang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-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

26 citing papers in PubMed, 57 citations in OpenAlex.

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  13. Gamma synuclein promotes cancer metastasis through the MKK3/6-p38MAPK cascade.International journal of biological sciences · 2022
    Article
  14. TGF-Frontiers in genetics · 2022
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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 2 institutions in 1 country.

Ting ShaoState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University and Collaboratory Inovation Center for Biotherapy, Chengdu, China.
Peiying SongState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University and Collaboratory Inovation Center for Biotherapy, Chengdu, China.
Hui HuaLaboratory of Stem Cell Biology, West China Hospital, Sichuan University, Chengdu, China.
Hongying ZhangState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University and Collaboratory Inovation Center for Biotherapy, Chengdu, China.
Xiangmin SunState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University and Collaboratory Inovation Center for Biotherapy, Chengdu, China.
Qingbin KongState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University and Collaboratory Inovation Center for Biotherapy, Chengdu, China.
Jiao WangSchool of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Ting LuoCancer Center, West China Hospital, Sichuan University, Chengdu, China.
Yangfu JiangState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University and Collaboratory Inovation Center for Biotherapy, Chengdu, China. jyangfu@scu.edu.cn.ORCID http://orcid.org/0000-0002-8696-2651
Sichuan University · CNChengdu University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor β (TGF-β) is critical for embryonic development, adult tissue homeostasis, and tumor progression. TGF-β suppresses tumors at early stage, but promotes metastasis at later stage through oncogenes such as Twist1. Gamma-synuclein (SNCG) is overexpressed in a variety of invasive and metastatic cancer. Here, we show that TGF-β induces SNCG expression by Smad-Twist1 axis, thus promoting TGF-β- and Twist1-induced cancer cell migration and invasion. We identify multiple Twist1-binding sites (E-boxes) in SNCG promoter. Chromatin immunoprecipitation and luciferase assays confirm the binding of Twist1 to the E-boxes of SNCG promoter sequence (-129/-1026 bp). Importantly, the Twist1-binding site close to the transcription initiation site is critical for the upregulation of SNCG expression by TGF-β and Twist1. Mutations of Twist1 motif on the SNCG promoter constructs markedly reduces the promoter activity. We further show that TGF-β induces Twist1 expression through Smad thereby enhancing the binding of Twist1 to SNCG promoter, upregulating SNCG promoter activity and increasing SNCG expression. SNCG knockdown abrogates TGF-β- or Twist1-induced cancer cell migration and invasion. Finally, SNCG knockdown inhibits the promotion of cancer metastasis by Twist1. Together, our data demonstrate that SNCG is a novel target of TGF-β-Smad-Twist1 axis and a mediator of Twist1-induced cancer metastasis.

Indexed as

Cell MovementE-Box Elementsgamma-SynucleinGene Expression Regulation, NeoplasticHeLa CellsHep G2 CellsHumansNeoplasm InvasivenessNeoplasm MetastasisNuclear ProteinsPromoter Regions, GeneticSmad ProteinsTransforming Growth Factor betaTwist-Related Protein 1Up-Regulationgamma-SynucleinNuclear ProteinsSmad ProteinsTransforming Growth Factor betaTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID29795373
PMCPMC5967338
OpenAlexW2804859499

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.