Evidence map›Paper›PMID 25430880›Full record

ArticleCancer gene therapy2014

Inhibition of Vav3 could reverse the drug resistance of gastric cancer cells by downregulating JNK signaling pathway.

B Tan, Y Li, Q Zhao, L Fan, Y Liu, D Wang, X Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Lactate Metabolism-Immune Regulation-Related Gene Signature in Lower-Grade Gliomas: Prognostic Model Development and Immune Characterization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Transcriptomic changes associated with DKK4 overexpression in pancreatic cancer cells detected by RNA-Seq.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. 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

7 authors at 2 institutions in 1 country.

B TanDepartment of General Surgery, the Fourth Affiliated Hospital, Hebei Medical University Shijiazhuang, Shijiazhuang, China.
Y LiDepartment of General Surgery, the Fourth Affiliated Hospital, Hebei Medical University Shijiazhuang, Shijiazhuang, China.
Q ZhaoDepartment of General Surgery, the Fourth Affiliated Hospital, Hebei Medical University Shijiazhuang, Shijiazhuang, China.
L FanDepartment of General Surgery, the Fourth Affiliated Hospital, Hebei Medical University Shijiazhuang, Shijiazhuang, China.
Y LiuDepartment of General Surgery, the Fourth Affiliated Hospital, Hebei Medical University Shijiazhuang, Shijiazhuang, China.
D WangDepartment of General Surgery, the Fourth Affiliated Hospital, Hebei Medical University Shijiazhuang, Shijiazhuang, China.
X ZhaoDepartment of General Surgery, the Fourth Affiliated Hospital, Hebei Medical University Shijiazhuang, Shijiazhuang, China.
Fourth Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aims to investigate the effect and mechanism of Vav3 on the multidrug resistance of gastric cancer. Fluorescence quantitative RT-PCR and western blot assay were used to detect Vav3 and drug resistance genes in gastric cancer tissues as well as gastric cell lines such as SGC7901, SGC7901/adriamycin (ADR) and GES-1. Besides, Vav3-specific small interfering RNA (Vav3-siRNA) was applied to inhibit Vav3 in SGC7901/ADR, and SRB assay was used to determine chemosensitivity. After that, drug resistance genes and proteins in MAPK and PI3K/AKT signaling pathway were detected after Vav3-siRNA transfection. The results showed that overexpressed Vav3 was found in gastric cancer tissues and SGC7901 and SGC7901/ADR cells. Activity of SGC7901/ADR cells transfected with Vav3-siRNA combined with 5-fluorouracil/oxaliplatin was much lower than that of control groups, and MDR1/P-gp, GST-π and Bcl-2, Bax genes were significantly downregulated in Vav3-siRNA transfection group. AKT, ERK and p38 total protein and their phosphorylation levels showed no significant change in Vav3-siRNA-transfected SGC7901/ADR cells, whereas the ratio of C-Jun phosphorylation levels to total C-Jun protein was significantly downregulated. The results suggested that Vav3 may play a role in drug resistance of gastric cancer by inhibiting drug resistance genes MDR1/P-gp, GST-π and Bcl-2 through regulating the JNK signaling pathway.

Indexed as

MAP Kinase Signaling SystemAdultAgedAntineoplastic AgentsCell Line, TumorDown-RegulationDrug Resistance, NeoplasmFemaleGene ExpressionGene Expression ProfilingGene Knockdown TechniquesGene SilencingHumansMaleMiddle AgedPhosphatidylinositol 3-KinasesAntineoplastic AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-vavRNA, Small InterferingVAV3 protein, human

Identifiers

PMID25430880
OpenAlexW1979774168

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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.