ArticleMolecular and cellular biochemistry2013
Ganglioside GM3 promotes HGF-stimulated motility of murine hepatoma cell through enhanced phosphorylation of cMet at specific tyrosine sites and PI3K/Akt-mediated migration signaling.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 27 citations in OpenAlex.
- Current state-of-the-art on ganglioside-mediated immune modulation in the tumor microenvironment.Cancer metastasis reviews · 2023Review
- Characterization of Lipid Alterations by OncogenicOmics : a journal of integrative biology · 2023Article
- GM3 synthase deficiency increases brain glucose metabolism in mice.Molecular genetics and metabolism · 2022Article
- Update on Glycosphingolipids Abundance in Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- AXL and MET in Hepatocellular Carcinoma: A Systematic Literature Review.Liver cancer · 2022Review
- Gangliosides as Signaling Regulators in Cancer.International journal of molecular sciences · 2021Review
- Induction of ganglioside synthesis in Drosophila brain accelerates assembly of amyloid β protein.Scientific reports · 2018Article
- Elongator promotes the migration and invasion of hepatocellular carcinoma cell by the phosphorylation of AKT.International journal of biological sciences · 2018Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ganglioside GM3 plays a well-documented and important role in the regulation of tumor cell proliferation, invasion, and metastasis by modulating tyrosine kinase growth factor receptors. However, the effect of GM3 on the hepatocyte growth factor receptor (HGFR, cMet) has not been fully delineated. In the current study, we investigated how GM3 affects cMet signaling and HGF-stimulated cell motility and migration using three hepatic cancer cell lines of mouse (Hca/A2, Hca/16A3, and Hepa1-6). Decreasing GM3 expression with the use of P4, a specific inhibitor for ganglioside synthesis inhibited the HGF-stimulated phosphorylation of cMet and activity of PI3K/Akt signaling pathway. In contrast, the increased expression of GM3 as a result of adding exogenous GM3 enhanced the HGF-stimulated phosphorylation of cMet and activity of PI3K/Akt signaling pathway. Furthermore, HGF-stimulated cell motility and migration in vitro were inhibited by reduced expression of GM3 and enhanced by increased expression of GM3. All the observations indicate that ganglioside GM3 promotes HGF-stimulated motility of murine hepatoma cell through enhanced phosphorylation of cMet at specific tyrosine sites and PI3K/Akt-mediated migration signaling.
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Registered trials
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.