Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Ganglioside GD3 promotes cell growth and invasion through p130Cas and paxillin in malignant melanoma cells.

Proceedings of the National Academy of Sciences of the United States of America - 2 Aug 2005

Hamamura Kazunori, Furukawa Keiko, Hayashi Takanori, Hattori Takeshi, Nakano Junji, Nakashima Hideyuki, Okuda Tetsuya, Mizutani Hideki, Hattori Hisashi, Ueda Minoru, Urano Takeshi, Lloyd Kenneth O, Furukawa Koichi

Abstract excerpt

Although ganglioside GD3 levels are highly elevated in malignant melanomas, the role of GD3 in melanomas' malignant properties has not been clearly shown. To investigate this problem, we genetically generated GD3-positive (GD3+) transfectant cells from a GD3-negative (GD3-) mutant line SK-MEL-28-N1 and analyzed the phenotypic changes in the transfected cells. GD3+ cells showed markedly increased cell growth and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Gangliosides
Share to Neoplasm Invasiveness

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Paxillin

Share to Phosphoproteins

Share to Retinoblastoma-Like Protein p130

Share to RNA, Small Interfering

Share to Sialyltransferases

Share to Tyrosine

Source

Open in PubMed Open full text

Identifiers

PMID: 16040804
DOI: 10.1073/pnas.0503658102
PMCID: PMC1180226

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Ganglioside GD3 promotes cell growth and invasion through p130Cas and paxillin in malignant melanoma cells.PMID 16040804Read ↗

Focal adhesion kinase as well as p130Cas and paxillin is crucially involved in the enhanced malignant properties under expression of ganglioside GD3 in melanoma cells.Semantic proximity Read ↗

Differential roles of gangliosides in malignant properties of melanomasSemantic proximity Read ↗

Disialyl gangliosides enhance tumor phenotypes with differential modalities.Semantic proximity Read ↗

Crucial roles of exosomes secreted from ganglioside GD3/GD2-positive glioma cells in enhancement of the malignant phenotypes and signals of GD3/GD2-negative glioma cells.Semantic proximity Read ↗

The biological role and immunotherapy of gangliosides and GD3 synthase in cancersSemantic proximity Read ↗

Ganglioside GD2 Enhances the Malignant Phenotypes of Melanoma Cells by Cooperating with Integrins.Semantic proximity Read ↗

B4GALNT1 induces angiogenesis, anchorage independence growth and motility, and promotes tumorigenesis in melanoma by induction of ganglioside GM2/GD2Semantic proximity Read ↗

Overexpression of caveolin-1 in a human melanoma cell line results in dispersion of ganglioside GD3 from lipid rafts and alteration of leading edges, leading to attenuation of malignant properties.Semantic proximity Read ↗

Alteration of tumor phenotypes of B16 melanoma after genetic remodeling of the ganglioside profile.Semantic proximity Read ↗

Upregulation of cell surface GD3 ganglioside phenotype is associated with human melanoma brain metastasis.Semantic proximity Read ↗

Lack of GD3 synthase (St8sia1) attenuates malignant properties of gliomas in genetically engineered mouse modelSemantic proximity Read ↗

Action Mechanisms of Exosomes Derived from GD3/GD2-Positive Glioma Cells in the Regulation of Phenotypes and Intracellular Signaling: Roles of Integrins.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.