Evidence map›Paper›PMID 27556509›Full record

ArticleOncotarget2016

Sphingosine-1-phosphate induced epithelial-mesenchymal transition of hepatocellular carcinoma via an MMP-7/ syndecan-1/TGF-β autocrine loop.

Ye Zeng, Xinghong Yao, Li Chen, Zhiping Yan, Jingxia Liu, Yingying Zhang, Tang Feng, Jiang Wu, Xiaoheng Liu

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

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  17. Metabolic Reprogramming of HCC: A New Microenvironment for Immune Responses.International journal of molecular sciences · 2023
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11 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

9 authors at 2 institutions in 1 country.

Ye ZengInstitute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China.
Xinghong YaoState Key Laboratory of Oncology in South China, Department of Radiation Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Li ChenState Key Laboratory of Oncology in South China, Department of Radiation Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Zhiping YanInstitute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China.
Jingxia LiuInstitute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China.
Yingying ZhangInstitute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China.
Tang FengInstitute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China.
Jiang WuInstitute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China.
Xiaoheng LiuInstitute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China.
Sichuan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingosine-1-phosphate (S1P) induces epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC). However, its underlying mechanism remains largely unknown. In the present study, we investigated the correlation between S1P and syndecan-1 in HCC, the molecular mechanism involved, as well as their roles in EMT of HCC. Results revealed a high serum S1P level presents in patients with HCC, which positively correlated with the serum syndecan-1 level. A significant inverse correlation existed between S1P1 and syndecan-1 in HCC tissues. S1P elicits activation of the PI3K/AKT signaling pathways via S1P1, which triggers HPSE, leading to increases in expression and activity of MMP-7 and leading to shedding and suppression of syndecan-1. The loss of syndecan-1 causes an increase in TGF-β1 production. The limited chronic increase in TGF-β1 can convert HCC cells into a mesenchymal phenotype via establishing an MMP-7/Syndecan-1/TGF-β autocrine loop. Finally, TGF-β1 and syndecan-1 are essential for S1P-induced epithelial to mesenchymal transition. Taken together, our study demonstrates that S1P induces advanced tumor phenotypes of HCC via establishing an MMP-7/syndecan-1/TGF-β1 autocrine loop, and implicates targetable S1P1-PI3K/AKT-HPSE-MMP-7 signaling axe in HCC metastasis.

Indexed as

AgedCarcinoma, HepatocellularCell Line, TumorEnzyme InhibitorsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsLysophospholipidsMaleMatrix Metalloproteinase 7Middle AgedPhenotypeSignal TransductionEnzyme InhibitorsLysophospholipidsMatrix Metalloproteinase 7MMP7 protein, humanSphingosinesphingosine 1-phosphateSyndecan-1TGFB1 protein, humanTransforming Growth Factor beta1epithelial-mesenchymal transitionhepatocellular carcinomasphingosine-1-phosphatesyndecan-1TGF-β

Identifiers

PMID27556509
PMCPMC5325366
OpenAlexW2509232842

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.