Evidence map›Paper›PMID 32239298›Full record

ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2020

Inhibiting the GAS6/AXL axis suppresses tumor progression by blocking the interaction between cancer-associated fibroblasts and cancer cells in gastric carcinoma.

Cheong A Bae, In-Hye Ham, Hye Jeong Oh, Dagyeong Lee, Jongsu Woo, Sang-Yong Son, Jung Hwan Yoon, James B Lorens, Rolf A Brekken, Tae-Min Kim and 3 more

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Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 44 citations in OpenAlex.

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  5. CD146Theranostics · 2026
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  13. Novel affibody molecules targeting the AXL extracellular structural domain for molecular imaging and targeted therapy of gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
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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

13 authors at 4 institutions in 3 countries.

Cheong A BaeDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea.
In-Hye HamDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea.
Hye Jeong OhDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea.
Dagyeong LeeDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea.
Jongsu WooDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea.
Sang-Yong SonDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea.
Jung Hwan YoonDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
James B LorensDepartment of Biomedicine, Centre for Cancer Biomarkers (CCBIO), University of Bergen, Bergen, Norway.
Rolf A BrekkenDivision of Surgical Oncology, Department of Surgery, Haman Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX, US.
Tae-Min KimDepartment of Medical Informatics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Sang-Uk HanDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea.
Won Sang ParkDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Hoon HurDepartment of Surgery, Ajou University School of Medicine, Cancer Biology Graduate Program, Ajou University Graduate School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon-si, Gyunggi-do, 16499, Republic of Korea. hhcmc75@ajou.ac.kr.
Ajou University · KRCatholic University of Korea · KRThe University of Texas Southwestern Medical Center · USUniversity of Bergen · NO

Funding

National Research Foundation of Korea 2019K1A3A1A20083809National Research Foundation of Korea 2019R1F1A1058915
6 · The paper itself

Abstract

backgroundThe effects of cancer-associated fibroblasts (CAF) on the progression of gastric carcinoma (GC) has recently been demonstrated. However, agents targeting the interaction between CAF and GC cells have not been applied in a clinical setting. Here, we examined if inhibition for Axl receptor tyrosine kinase (AXL) can suppress CAF-induced aggressive phenotype in GC.

methodsWe investigated the function of CAF-derived growth arrest-specific 6 (GAS6), a major ligand of AXL, on the migration and proliferation of GC cells. The effect of the AXL inhibitor, BGB324, on the CAF-induced aggressive phenotype of GC cells was also investigated. In addition, we performed immunohistochemistry to examine the expression of phosphorylated AXL protein in 175 GC tissues and evaluated its correlation with the prognosis.

resultsThe qPCR and western blot analysis showed that GAS6 expression was higher in CAF relative to other cells. We found that co-culture with CAF increased the phosphorylation of AXL (P-AXL), differentiation into a mesenchymal-like phenotype, and cell survival in GC cell lines. When the expression of AXL was genetically inhibited in GC cells, the effect of CAF was reduced. BGB324, a small molecule inhibitor of AXL, suppressed the effects of CAF on GC cell lines. In GC tissues, high levels of P-AXL were significantly associated with poor overall survival (P = 0.022).

conclusionsWe concluded that CAF are a major source of GAS6 and that GAS6 promotes an aggressiveness through AXL activation in GC. We suggested that an AXL inhibitor may be a novel agent for GC treatment.

Indexed as

Axl Receptor Tyrosine KinaseBenzocycloheptenesBiomarkers, TumorCancer-Associated FibroblastsCell ProliferationCell SurvivalDisease ProgressionGene Expression Regulation, NeoplasticGrowth Arrest-Specific Protein 6HumansIntercellular Signaling Peptides and ProteinsPhosphorylationPrognosisProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesStomach NeoplasmsAXL protein, humanAxl Receptor Tyrosine KinasebemcentinibBenzocycloheptenesBiomarkers, TumorGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTriazolesAXLCancer-associated fibroblastsGAS6Gastric cancerTumor microenvironment

Identifiers

PMID32239298
OpenAlexW3014147786

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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.