Evidence map›Paper›PMID 39457390›Full record

ArticleGenes2024

The VEGFA-Induced MAPK-AKT/PTEN/TGFβ Signal Pathway Enhances Progression and MDR in Gastric Cancer.

Hongming Fang, Yujuan Zhou, Xue Bai, Wanlin Che, Wenxuan Zhang, Danying Zhang, Qingmei Chen, Wei Duan, Guochao Nie, Yingchun Hou

Abstract read
In one paragraph

Article in Genes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Therapeutic potential of targeting macrophage polarization in metastatic gastric cancer: a review on core mechanisms and clinical progress.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  3. Article
  4. Article
  5. Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025
    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

10 authors.

Hongming FangCollege of Life Sciences, Shaanxi Normal University, 620 West Chang-An Street, Xi'an 710119, China.ORCID 0009-0007-0426-2445
Yujuan ZhouCollege of Life Sciences, Shaanxi Normal University, 620 West Chang-An Street, Xi'an 710119, China.
Xue BaiCollege of Life Sciences, Shaanxi Normal University, 620 West Chang-An Street, Xi'an 710119, China.
Wanlin CheCollege of Life Sciences, Shaanxi Normal University, 620 West Chang-An Street, Xi'an 710119, China.
Wenxuan ZhangCollege of Life Sciences, Shaanxi Normal University, 620 West Chang-An Street, Xi'an 710119, China.
Danying ZhangCollege of Life Sciences, Shaanxi Normal University, 620 West Chang-An Street, Xi'an 710119, China.
Qingmei ChenGuangxi Key Laboratory of Agricultural Resource Chemistry and Biotechnology, 299 Jiao-Yu-Zhong Road, Yulin 537000, China.ORCID 0009-0006-0967-1718
Wei DuanSchool of Medicine, Deakin University, and IMPACT Strategic Research Centre, Melbourne, VIC 3216, Australia.
Guochao NieGuangxi Key Laboratory of Agricultural Resource Chemistry and Biotechnology, 299 Jiao-Yu-Zhong Road, Yulin 537000, China.
Yingchun HouCollege of Life Sciences, Shaanxi Normal University, 620 West Chang-An Street, Xi'an 710119, China.

Funding

G Nie No. Guike AA20302013G Nie No. RC20200001G Nie "Yongjiang Plan" Project of Leading Talents of Innovation and Entrepreneurship in Nanning City
6 · The paper itself

Abstract

BACKGROUND/

objectivesGastric cancer (GC) is a globally frequent cancer, in particular leading in mortality caused by digestive tract cancers in China. Vascular endothelial growth factor A (VEGFA) is excessively expressed in cancers including GC; its involvement in GC development, particularly in multidrug resistance (MDR), and the signal route it affects in GC remain unknown. To explore the roles VEGFA plays during progression and MDR formation in GC, we studied its function in a VEGFA-deleted GC cell platform.

methodsWe initially assessed the importance of VEGFA in GC and MDR using database analysis. Then, using CCK8, wound healing, transwell, scanning electron microscopy, immunofluorescence, flow cytometry, and other techniques, the alterations in tumor malignancy-connected cell behaviors and microstructures were photographed and evaluated in a VEGFA-gene-deleted GC cell line (VEGFA-/-SGC7901). Finally, the mechanism of VEGFA in GC progression and MDR was examined by Western blot.

resultsDatabase analysis revealed a strong correlation between high VEGFA expression and a poor prognosis for GC. The results showed that VEGFA deletion reduced GC cell proliferation and motility and altered microstructures important for motility, such as the depolymerized cytoskeleton. VEGFA deletion inhibited the growth of pseudopodia/filopodia and suppressed the epithelial-mesenchymal transition (EMT). The occurrence of MDR is induced by overactivation of the MAPK-AKT and TGFβ signaling pathways, while PTEN inhibits these pathways.

conclusionsAll findings suggested that VEGFA acts as a cancer enhancer and MDR inducer in GC via the MAPK-AKT/PTEN/TGFβ signal pathway.

Indexed as

Drug Resistance, MultipleDrug Resistance, NeoplasmProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionStomach NeoplasmsTransforming Growth Factor betaVascular Endothelial Growth Factor ACell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTransforming Growth Factor betaVascular Endothelial Growth Factor AVEGFA protein, humangastric cancerMAPKMDRPTENTGFβVEGFA

Identifiers

PMID39457390
PMCPMC11507385

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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.