Evidence map›Paper›PMID 28112190›Full record

ArticleScientific reports2017

Up-regulation of syncytin-1 contributes to TNF-α-enhanced fusion between OSCC and HUVECs partly via Wnt/β-catenin-dependent pathway.

Ting-Lin Yan, Meng Wang, Zhi Xu, Chun-Ming Huang, Xiao-Cheng Zhou, Er-Hui Jiang, Xiao-Ping Zhao, Yong Song, Kai Song, Zhe Shao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. The double-positive cells in the tumor microenvironment.Journal of translational internal medicine · 2026
    Article
  3. Review
  4. How Do Cancer Cells Fuse and Why?Advances in experimental medicine and biology · 2026
    Review
  5. Implications of Heterotypic Cell Fusion in Cancer.Advances in experimental medicine and biology · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Cell-cell fusion in cancer: The next cancer hallmark?The international journal of biochemistry & cell biology · 2024
    Review
  10. Article
  11. Article
  12. Cell Fusion and Syncytia Formation in Cancer.Results and problems in cell differentiation · 2024
    Review
  13. Mechanisms of Cell Fusion in Cancer.Results and problems in cell differentiation · 2024
    Review
  14. Article
  15. Intrinsic signalling factors associated with cancer cell-cell fusion.Cell communication and signaling : CCS · 2023
    Review
  16. Extracellular Events Involved in Cancer Cell-Cell Fusion.International journal of molecular sciences · 2022
    Review
  17. Generation of Cancer Stem/Initiating Cells by Cell-Cell Fusion.International journal of molecular sciences · 2022
    Review
  18. Overexpression of PTPRZ1 Regulates p120/Journal of oncology · 2022
    Article
  19. Review
  20. Review
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

12 authors at 4 institutions in 1 country.

Ting-Lin YanThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Meng WangThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Zhi XuThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Chun-Ming HuangThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Xiao-Cheng ZhouThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Er-Hui JiangThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Xiao-Ping ZhaoCenter of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yong SongDepartment of Stomatology, Liuzhou People's Hospital, Guangxi, China.
Kai SongDepartment of Oral and Maxillofacial Surgery, The Affliated Hospital of Qingdao University, Qingdao, China.
Zhe ShaoThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Ke LiuThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Zheng-Jun ShangThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) &Key Laboratory for Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.
Wuhan University · CNLiuzhou General Hospital · CNQingdao University · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence implies that cell fusion is one of the driving forces of cancer invasion and metastasis. However, considerably less is still known about the triggering factors and underlying mechanisms associated with cancer-host cell fusion, particularly in inflammatory tumor microenvironment. In this study, we confirmed that inflammatory factor TNF-α could enhance fusion between squamous cell carcinoma cells 9 (SCC-9) and human umbilical vein endothelial cells (HUVEC). Further study revealed that TNF-α could promote up-regulation of syncytin-1 in SCC-9 and its receptor neutral amino acid transporter type 2 (ASCT-2) in HUVEC. Syncytin-1 acted as an important downstream effector in TNF-α-enhanced cancer-endothelial cell fusion. TNF-α treatment also led to the activation of Wnt/β-catenin signal pathway in SCC-9. The activation of Wnt/β-catenin signal pathway was closely associated with the up-regulation of syncytin-1 in SCC-9 and increased fusion between SCC-9 and HUVEC while blocking of Wnt/β-catenin signal pathway resulted in the corresponding down-regulation of syncytin-1 accompanied by sharp decrease of cancer-endothelial cell fusion. Taking together, our results suggest that Wnt/β-catenin signal pathway activation-dependent up-regulation of syncytin-1 contributes to the pro-inflammatory factor TNF-α-enhanced fusion between oral squamous cell carcinoma cells and endothelial cells.

Indexed as

Cell FusionWnt Signaling PathwayAmino Acid Transport System ASCbeta CateninCell LineEndothelial CellsEpithelial CellsGene Products, envHumansMinor Histocompatibility AntigensPregnancy ProteinsTumor Necrosis Factor-alphaUp-RegulationAmino Acid Transport System ASCbeta CateninGene Products, envMinor Histocompatibility AntigensPregnancy ProteinsSLC1A5 protein, humansyncytinTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID28112190
PMCPMC5256027
OpenAlexW2580194217

What OpenQuestion holds

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Registered trials

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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.