Evidence map›Paper›PMID 34035222›Full record

ArticleSignal transduction and targeted therapy2021

Exosomal S100A4 derived from highly metastatic hepatocellular carcinoma cells promotes metastasis by activating STAT3.

Haoting Sun, Chaoqun Wang, Beiyuan Hu, Xiaomei Gao, Tiantian Zou, Qin Luo, Mo Chen, Yan Fu, Yuanyuan Sheng, Kaili Zhang and 7 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
6.7field-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

78 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
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  5. ADCY7 dictates N-cadherin stability to inhibit HCC metastasis.JHEP reports : innovation in hepatology · 2026
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18 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

17 authors at 1 institution in 1 country.

Haoting Sun *Department of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Chaoqun Wang *Department of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Beiyuan Hu *Department of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Xiaomei Gao *Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Tiantian ZouDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Qin LuoInstitutes of Biomedical Sciences, Fudan University, Shanghai, China.
Mo ChenDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Yan FuDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Yuanyuan ShengInstitutes of Biomedical Sciences, Fudan University, Shanghai, China.
Kaili ZhangInstitutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yan ZhengInstitutes of Biomedical Sciences, Fudan University, Shanghai, China.
Xudong RenDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Shican YanDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Yan GengDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Luyu YangDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China.
Qiongzhu DongDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China. qzhdong@fudan.edu.cn.ORCID 0000-0002-2433-7199
Lunxiu QinDepartment of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, Shanghai, China. qinlx@fudan.edu.cn.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intercellular cross-talk plays important roles in cancer progression and metastasis. Yet how these cancer cells interact with each other is still largely unknown. Exosomes released by tumor cells have been proved to be effective cell-to-cell signal mediators. We explored the functional roles of exosomes in metastasis and the potential prognostic values for hepatocellular carcinoma (HCC). Exosomes were extracted from HCC cells of different metastatic potentials. The metastatic effects of exosomes derived from highly metastatic HCC cells (HMH) were evaluated both in vitro and in vivo. Exosomal proteins were identified with iTRAQ mass spectrum and verified in cell lines, xenograft tumor samples, and functional analyses. Exosomes released by HMH significantly enhanced the in vitro invasion and in vivo metastasis of low metastatic HCC cells (LMH). S100 calcium-binding protein A4 (S100A4) was identified as a functional factor in exosomes derived from HMH. S100A4

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionExosomesFemaleGene Expression Regulation, NeoplasticHeterograftsHumansLiver NeoplasmsMaleMiceMiddle AgedNeoplasm MetastasisOsteopontinS100A4 protein, humanS100 Calcium-Binding Protein A4STAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID34035222
PMCPMC8149717
OpenAlexW3164644487

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.