Evidence map›Paper›PMID 25628786›Full record

ArticleAmerican journal of translational research2014

STAT3 regulation the expression of VEGF-D in HGC-27 gastric cancer cell.

Jingyu Deng, Jingli Cui, Nan Jiang, Rupeng Zhang, Li Zhang, Xishan Hao, Han Liang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of the VEGF Family in Coronary Heart Disease.Frontiers in cardiovascular medicine · 2021
    Review
  4. Article
  5. Article
  6. Review
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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

7 authors at 1 institution in 1 country.

Jingyu DengDepartment of Gastroenterology, Tianjin Medical University Cancer Hospital and City Key Laboratory of Cancer Prevention and Therapy, Nation Clinical Center of Cancer Tianjin, China.
Jingli CuiDepartment of Gastroenterology, Tianjin Medical University Cancer Hospital and City Key Laboratory of Cancer Prevention and Therapy, Nation Clinical Center of Cancer Tianjin, China.
Nan JiangDepartment of Gastroenterology, Tianjin Medical University Cancer Hospital and City Key Laboratory of Cancer Prevention and Therapy, Nation Clinical Center of Cancer Tianjin, China.
Rupeng ZhangDepartment of Gastroenterology, Tianjin Medical University Cancer Hospital and City Key Laboratory of Cancer Prevention and Therapy, Nation Clinical Center of Cancer Tianjin, China.
Li ZhangDepartment of Gastroenterology, Tianjin Medical University Cancer Hospital and City Key Laboratory of Cancer Prevention and Therapy, Nation Clinical Center of Cancer Tianjin, China.
Xishan HaoDepartment of Gastroenterology, Tianjin Medical University Cancer Hospital and City Key Laboratory of Cancer Prevention and Therapy, Nation Clinical Center of Cancer Tianjin, China.
Han LiangDepartment of Gastroenterology, Tianjin Medical University Cancer Hospital and City Key Laboratory of Cancer Prevention and Therapy, Nation Clinical Center of Cancer Tianjin, China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the potential mechanism of vascular endothelial growth factor D (VEGF-D) contribution to the lymphangiogenesis was regulated by the signal transducer and activator of transcription 3 (STAT3).

methodsWe detected the expression in GC tissue, adjacent non-tumor tissue, GC cell lines (AGS, SUN-1, KATO-III, BGC-823, MGC-803, SGC-7901, and HGC-27), and GES-1 cell line. STAT3 siRNA transfection and genome microarray were applied to demonstrate whether the expression of VEGF-D was mediated by the STAT3 in GC.

resultsWe showed the STAT3, pSTAT3, and VEGF-D expression in GC tissue was significantly higher than those in adjacent non-tumor tissue, respectively. In addition, both STAT3 and VEGF-D mRNA expression was much higher in each GC cell line than those in GES-1 cell line. With STAT3 siRNA transfection, we demonstrated that VEGF-D expression level decreased significantly in HGC-27 cell by using the genome microarray representing STAT3 potential regulation the VEGF-D expression.

conclusionSTAT3, a novel signal transducer inactivating in the GC cell, can contribute to the lymph node metastasis by promoting lymphangiogenesis via up-regulation expression of VEGF-D.

Indexed as

lymphatic metastasisneoplasmsignal transducer and activator of transcription 3Stomachvascular endothelial growth factor

Identifiers

PMID25628786
PMCPMC4297343
OpenAlexW2413678010

What OpenQuestion holds

Textmetadata
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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.