Evidence map›Paper›PMID 25080937›Full record

ArticleCell death and differentiation2014

SRF expedites metastasis and modulates the epithelial to mesenchymal transition by regulating miR-199a-5p expression in human gastric cancer.

X Zhao, L He, T Li, Y Lu, Y Miao, S Liang, H Guo, M Bai, H Xie, G Luo and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.8field-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

62 citing papers in PubMed, 94 citations in OpenAlex.

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  16. Prognostic Value of LHFPL Tetraspan Subfamily Member 6Pharmacogenomics and personalized medicine · 2021
    Article
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2 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

18 authors at 3 institutions in 1 country.

X ZhaoState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
L He1] State Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China [2] Department of Nephrology, Xijing Hospital, the Fourth Military Medical University, Xi'an, Shaanxi, China.
T LiState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
Y LuState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
Y Miao1] State Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China [2] Department of Gastroenterology, the People's Hospital of Ningxia Hui Nationality Autonomous Region, Yinchuan, Ningxia Hui Autonomous Region, China.
S LiangState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
H GuoState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
M BaiState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
H XieState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
G LuoState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
L ZhouState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
G ShenState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
C GuoState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
F BaiDepartment of Gastroenterology, the People's Hospital of Ningxia Hui Nationality Autonomous Region, Yinchuan, Ningxia Hui Autonomous Region, China.
S SunDepartment of Nephrology, Xijing Hospital, the Fourth Military Medical University, Xi'an, Shaanxi, China.
K WuState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
Y NieState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
D FanState Key Laboratory of Cancer Biology & Institute of Digestive Diseases, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Xi'an, Shaanxi, China.
Air Force Medical University · CNXijing Hospital · CNThe Fourth People's Hospital of Ningxia Hui Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of transcription factors (TFs) is associated with tumor progression, but little is known about TF expression patterns in the context of gastric cancer (GC) metastasis. Using array-based profile analysis, we found that 22 TFs showed differential activities between GC cell lines with low- and high-metastatic potential. Of this group of TFs, serum response factor (SRF) was significantly upregulated in metastatic GC cells. SRF expression was frequently elevated in a panel of metastatic GC cells and tissues, and high-level expression of SRF was significantly associated with a more aggressive phenotype and poor prognosis in patients with GC. In GC cell lines, overexpression of SRF potently promoted cell migration and invasion in vitro as well as the formation of intrahepatic and pulmonary metastases in vivo, whereas loss of SRF inhibited GC cell invasion and metastasis. We also performed a microRNA microarray to screen for transcriptional targets of SRF and found that SRF transactivates miR-199a-5p and miR-199a-3p by directly binding to their promoters. We further determined that overexpression of miR-199a-5p, but not miR-199a-3p, increased GC cell invasion and metastasis. In contrast, inhibition of miR-199a-5p impaired the metastatic potential of GC cells in vitro and in vivo, and E-cadherin was identified as a direct and functional target of miR-199a-5p in GC cells. Specifically, our results showed that SRF promotes GC metastasis and the epithelial to mesenchymal transition (EMT) though miR-199a-5p-mediated downregulation of E-cadherin. The present study thus provides insight into the specific biological behavior of SRF in GC metastasis. As increased activity of the SRF/miR-199a-5p/E-cadherin pathway appears to promote GC cell EMT and metastasis, these regulators may therefore be developed as therapeutic targets or biomarkers for GC progression.

Indexed as

Epithelial-Mesenchymal TransitionAntigens, CDBase SequenceBinding SitesCadherinsCell AdhesionCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansLymphatic MetastasisMaleMicroRNAsMiddle AgedNeoplasm InvasivenessPromoter Regions, GeneticAntigens, CDCadherinsCDH1 protein, humanMicroRNAsmirn199 microRNA, humanSerum Response FactorSRF protein, human

Identifiers

PMID25080937
PMCPMC4227147
OpenAlexW2060950997

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.