Evidence map›Paper›PMID 24841138›Full record

ArticleOncology reports2014

Role of c-Src activity in the regulation of gastric cancer cell migration.

Yun Yang, Zhi-Gang Bai, Jie Yin, Guo-Cong Wu, Zhong-Tao Zhang

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Cancers · 2022
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  6. Updates on mechanistic insights and targeting of tumour metastasis.Journal of cellular and molecular medicine · 2020
    Review
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  14. Article
  15. Article
  16. The up-regulation of miR-300 in gastric cancer and its effects on cells malignancy.International journal of clinical and experimental medicine · 2015
    Article
  17. Article
  18. MicroRNA-126 regulates migration and invasion of gastric cancer by targeting CADM1.International journal of clinical and experimental pathology · 2015
    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

5 authors at 2 institutions in 1 country.

Yun YangDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, Xuanwu, Beijing 100050, P.R. China.
Zhi-Gang BaiDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, Xuanwu, Beijing 100050, P.R. China.
Jie YinDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, Xuanwu, Beijing 100050, P.R. China.
Guo-Cong WuDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, Xuanwu, Beijing 100050, P.R. China.
Zhong-Tao ZhangDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, Xuanwu, Beijing 100050, P.R. China.
Capital Medical University · CNBeijing Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer is associated with increased migration and invasion. In the present study, we explored the role of c-Src in gastric cancer cell migration and invasion. BGC-823 gastric cancer cells were used to investigate migration following treatment of these cells with the c-Src inhibitors, PP2 and SU6656. Migration and invasion were analyzed by wound healing and Transwell assays. Western blot analysis was used to detect the expression of MT1-MMP and VEGF-C, while the activity of MMP2 and MMP9 was monitored with gelatin zymography assay. Immunoprecipitation was used to detect interactions among furin, pro-MT1-MMP and pro-VEGF-C. MT1-MMP and VEGF-C expression levels were inhibited by PP2 and SU6656 treatment, in accordance with decreased c-Src activity. Similarly, the zymography assay demonstrated that the activity of MMP2 and MMP9 was decreased following PP2 or SU6656 treatment. Blockade of c-Src also inhibited the invasive and migratory capacity of BGC-823 cells. Notably, c-Src interacted with furin in vivo, while interactions between furin and its substrates, pro-MT1-MMP and pro-VEGF-C, were decreased by c-Src inhibitors. In conclusion, the interaction among furin and pro-MT1-MMP or pro-VEGF-C or other tumor-associated precursor enzymes can be regulated by c-Src activity, thus reducing or changing the expression of these enzymes in order to reduce the development of gastric cancer, invasion and metastasis.

Indexed as

Cell Line, TumorCell MovementCSK Tyrosine-Protein KinaseFurinGene Expression Regulation, NeoplasticHumansIndolesMatrix Metalloproteinase 14Neoplasm InvasivenessPyrimidinessrc-Family KinasesStomach NeoplasmsSulfonamidesVascular Endothelial Growth Factor CAG 1879CSK protein, humanCSK Tyrosine-Protein KinaseFurinFURIN protein, humanIndolesMatrix Metalloproteinase 14Pyrimidinessrc-Family KinasesSU 6656SulfonamidesVascular Endothelial Growth Factor C

Identifiers

PMID24841138
PMCPMC4067425
OpenAlexW2045711935

What OpenQuestion holds

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LicenceCC BY
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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.