Evidence map›Paper›PMID 28432277›Full record

ArticleOncotarget2017

Transforming growth factor β1 promotes invasion of human JEG-3 trophoblast cells via TGF-β/Smad3 signaling pathway.

Zhongying Huang, Shangwei Li, Wei Fan, Qianhong Ma

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  4. The Role of TGF-β during Pregnancy and Pregnancy Complications.International journal of molecular sciences · 2023
    Review
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  6. Article
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  20. Hypoxia-Induced Activation of JAK/STAT3 Signaling Pathway Promotes Trophoblast Cell Viability and Angiogenesis in Preeclampsia.Medical science monitor : international medical journal of experimental and clinical research · 2017
    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

4 authors at 1 institution in 1 country.

Zhongying HuangDepartment of Obsterics and Gynecology, West China 2nd Hospital, University of Sichuan, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, Chengdu 610041, People's Republic of China.
Shangwei LiDepartment of Obsterics and Gynecology, West China 2nd Hospital, University of Sichuan, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, Chengdu 610041, People's Republic of China.
Wei FanDepartment of Obsterics and Gynecology, West China 2nd Hospital, University of Sichuan, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, Chengdu 610041, People's Republic of China.
Qianhong MaDepartment of Obsterics and Gynecology, West China 2nd Hospital, University of Sichuan, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, Chengdu 610041, People's Republic of China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-β1 is involved invasion of human trophoblasts. However, the underlying mechanisms remain unclear. In this study, we performed Transwell assay and found that TGF-β1 promoted the invasion of trophoblast cell line JEG-3. Treatment with TGF-β1 up-regulated the expression of receptor-regulated Smad transcription factors Smad2 and Smad3, and two invasive-associated genes, namely, matrix metallopeptidase (MMP)-9 and MMP-2, in JEG-3 cells. Over-expressing activin receptor-like kinase (ALK) 5, the TGF-β type I receptor (TβRI) enhanced the up-regulation of Smad2, Smad3, MMP-9, and MMP-2 induced by TGF-β1, whereas application of TβRI inhibitor SB431542 diminished the stimulatory effects of TGF-β1 on these genes. Furthermore, transfection of Smad3 and ALK-5 seperately or in combination into JEG-3 cells before TGF-β1 treatment significantly increased the expression of MMP-9 and MMP-2. By contrast, silencing Smad3 and Smad2 by siRNAs significantly decreased the expression of MMP-9 and MMP-2, with Smad3 silence having a more potent inhibitory effect. Inhibiting TβRI with SB431542 or knockdown of Smad3, but not Smad2, abolished the stimulatory effect of TGF-β1 on the invasion of JEG-3 cells. Taken together, the results indicate that TGF-β1 activates the Smads signaling pathway in JEG-3 trophoblast cells and Smad3 play a key role in TGF-β1-induced invasion of JEG-3 and up-regulation of MMP-9 and MMP-2 expression.

Indexed as

Signal TransductionCell Line, TumorGene Expression Regulation, NeoplasticHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9Smad3 ProteinTransforming Growth Factor betaTransforming Growth Factor beta1TrophoblastsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Smad3 ProteinSMAD3 protein, humanTransforming Growth Factor betaTransforming Growth Factor beta1matrix metalloproteinasesSmadsTGF-β signalingtrophoblast

Identifiers

PMID28432277
PMCPMC5464890
OpenAlexW2605283411

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.