Evidence map›Paper›PMID 35008849›Full record

ArticleInternational journal of molecular sciences2021

Ganglioside GD2 Enhances the Malignant Phenotypes of Melanoma Cells by Cooperating with Integrins.

Farhana Yesmin, Robiul H Bhuiyan, Yuhsuke Ohmi, Satoko Yamamoto, Kei Kaneko, Yuki Ohkawa, Pu Zhang, Kazunori Hamamura, Nai-Kong V Cheung, Norihiro Kotani and 6 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  8. Strategies to manage the adverse effects of immunotherapy with dinutuximab beta in neuroblastoma: an Italian experience and literature review.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 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

16 authors at 6 institutions in 2 countries.

Farhana YesminDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Robiul H BhuiyanDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.ORCID 0000-0003-3193-1783
Yuhsuke OhmiDepartment of Medical Technology, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Satoko YamamotoDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Kei KanekoDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Yuki OhkawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Pu ZhangDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Kazunori HamamuraDepartment of Pharmacology, Aichi Gakuin University School of Dentistry, Nagoya 464-8650, Japan.ORCID 0000-0002-8143-338X
Nai-Kong V CheungMemorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0001-6323-5171
Norihiro KotaniDepartment of Biochemistry, Saitama Medical University, Saitama 350-0495, Japan.
Koichi HonkeDepartment of Biochemistry, Kochi University School of Medicine, Nangoku 783-8505, Japan.ORCID 0000-0002-6123-7576
Tetsuya OkajimaDepartment of Molecular Biochemistry, Nagoya University Graduate School of Medicine, Nagoya 466-0065, Japan.ORCID 0000-0002-3677-648X
Mariko KambeDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Orie TajimaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Keiko FurukawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.
Koichi FurukawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai 487-8501, Japan.ORCID 0000-0002-3321-9784
Chubu University · JPAichi Gakuin University · JPKōchi University · JPMemorial Sloan Kettering Cancer Center · USNagoya University · JPSaitama Medical University · JP

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
JST-CREST JPMJCR17H2Ministry of Education, Culture, Sports and Technology of Japan 15H04696, 17K19616, 18H02628, 19K22518, 21K06828, 21H026NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Gangliosides have been considered to modulate cell signals in the microdomain of the cell membrane, lipid/rafts, or glycolipid-enriched microdomain/rafts (GEM/rafts). In particular, cancer-associated gangliosides were reported to enhance the malignant properties of cancer cells. In fact, GD2-positive (GD2+) cells showed increased proliferation, invasion, and adhesion, compared with GD2-negative (GD2-) cells. However, the precise mechanisms by which gangliosides regulate cell signaling in GEM/rafts are not well understood. In order to analyze the roles of ganglioside GD2 in the malignant properties of melanoma cells, we searched for GD2-associating molecules on the cell membrane using the enzyme-mediated activation of radical sources combined with mass spectrometry, and integrin β1 was identified as a representative GD2-associating molecule. Then, we showed the physical association of GD2 and integrin β1 by immunoprecipitation/immunoblotting. Close localization was also shown by immuno-cytostaining and the proximity ligation assay. During cell adhesion, GD2+ cells showed multiple phospho-tyrosine bands, i.e., the epithelial growth factor receptor and focal adhesion kinase. The knockdown of integrin β1 revealed that the increased malignant phenotypes in GD2+ cells were clearly cancelled. Furthermore, the phosphor-tyrosine bands detected during the adhesion of GD2+ cells almost completely disappeared after the knockdown of integrin β1. Finally, immunoblotting to examine the intracellular distribution of integrins during cell adhesion revealed that large amounts of integrin β1 were localized in GEM/raft fractions in GD2+ cells before and just after cell adhesion, with the majority being localized in the non-raft fractions in GD2- cells. All these results suggest that GD2 and integrin β1 cooperate in GEM/rafts, leading to enhanced malignant phenotypes of melanomas.

Indexed as

AnimalsAntibodies, MonoclonalCell AdhesionCell Line, TumorCell ProliferationCollagen Type IGangliosidesHumansIntegrin beta1IntegrinsMass SpectrometryMelanomaMembrane MicrodomainsMicePhenotypePhosphotyrosineAntibodies, MonoclonalCollagen Type Iganglioside, GD2GangliosidesIntegrin beta1IntegrinsPhosphotyrosinecancer-associated antigengangliosideGEM/raftsintegrinmelanoma

Identifiers

PMID35008849
PMCPMC8745508
OpenAlexW4205739680

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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.