Evidence map›Paper›PMID 27986811›Full record

ArticleThe Journal of biological chemistry2017

EphB3 Stimulates Cell Migration and Metastasis in a Kinase-dependent Manner through Vav2-Rho GTPase Axis in Papillary Thyroid Cancer.

Jing-Jing Li, Zhi-Jian Sun, Yan-Mei Yuan, Fen-Fen Yin, Yao-Gang Bian, Ling-Yun Long, Xue-Li Zhang, Dong Xie

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. The role of EphA7 in different tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  9. Article
  10. Knockdown ofTranslational cancer research · 2022
    Article
  11. Article
  12. Targeting Rac and Cdc42 GEFs in Metastatic Cancer.Frontiers in cell and developmental biology · 2020
    Review
  13. Article
  14. BRAFEndocrine · 2019
    Article
  15. Article
  16. 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

8 authors at 3 institutions in 1 country.

Jing-Jing LiFrom the Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China and.
Zhi-Jian SunFrom the Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China and.
Yan-Mei YuanFrom the Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China and.
Fen-Fen YinFrom the Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China and.
Yao-Gang Bianthe Department of General Surgery, Fengxian Hospital Affiliated to Southern Medical University, 6600 Nanfeng Road, Shanghai 201499, China.
Ling-Yun LongFrom the Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China and.
Xue-Li Zhangthe Department of General Surgery, Fengxian Hospital Affiliated to Southern Medical University, 6600 Nanfeng Road, Shanghai 201499, China lejing1996@aliyun.com.
Dong XieFrom the Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China and dxie@sibs.ac.cn.
Shanghai Institutes for Biological Sciences · CNSouthern Medical University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eph receptors, the largest subfamily of transmembrane tyrosine kinase receptors, have been increasingly implicated in various physiologic and pathologic processes, and the roles of the Eph family members during tumorigenesis have recently attracted growing attentions. In the present study, we explored the function of EphB3, one member of Eph family, in papillary thyroid cancer (PTC). We found that the expression of EphB3 was significantly elevated in PTC. Either overexpression of EphB3 or activation of EphB3 by EfnB1-Fc/EfnB2-Fc stimulated in vitro migration of PTC cells. In contrast, siRNA-mediated knockdown of EphB3 or EphB3-Fc treatment, which only blocked EphB3-mediated forward signaling, inhibited migration and metastasis of PTC cells. A mechanism study revealed that EphB3 knockdown led to suppressed activity of Rac1 and enhanced activity of RhoA. Moreover, we found that Vav2, an important regulator of Rho family GTPases, was activated by EphB3 in a kinase-dependent manner. Altogether, our work suggested that EphB3 acted as a tumor promoter in PTC by increasing the in vitro migration as well as the in vivo metastasis of PTC cells through regulating the activities of Vav2 and Rho GTPases in a kinase-dependent manner.

Indexed as

Cell MovementGene Expression Regulation, NeoplasticCarcinomaCarcinoma, PapillaryCell Line, TumorFemaleHumansMaleNeoplasm MetastasisProto-Oncogene Proteins c-vavrac1 GTP-Binding ProteinReceptor, EphB3Signal TransductionThyroid Cancer, PapillaryThyroid NeoplasmsProto-Oncogene Proteins c-vavrac1 GTP-Binding ProteinRAC1 protein, humanReceptor, EphB3VAV2 protein, humancancer biologycell migrationEphB3focal adhesionmetastasispapillary thyroid cancerRho (Rho GTPase)Vav2

Identifiers

PMID27986811
PMCPMC5247645
OpenAlexW2564245727

What OpenQuestion holds

Textmetadata
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.