VEGF-A promotes the motility of human melanoma cells through the VEGFR1-PI3K/Akt signaling pathway.
Animals
Antibodies, Neutralizing
/ pharmacology
Cell Movement
/ genetics
Humans
Melanoma
/ genetics
Oligonucleotides, Antisense
/ pharmacology
Phosphatidylinositol 3-Kinase
/ metabolism
Phosphatidylinositol 3-Kinases
/ metabolism
Phosphatidylinositols
/ pharmacology
Proto-Oncogene Proteins c-akt
/ metabolism
Signal Transduction
Vascular Endothelial Growth Factor A
/ metabolism
Wortmannin
/ pharmacology
Cell motility
Melanoma
PI3K/Akt signaling pathway
VEGF-A
VEGFR1
Journal
In vitro cellular & developmental biology. Animal
ISSN: 1543-706X
Titre abrégé: In Vitro Cell Dev Biol Anim
Pays: Germany
ID NLM: 9418515
Informations de publication
Date de publication:
Sep 2022
Sep 2022
Historique:
received:
13
07
2022
accepted:
12
08
2022
pubmed:
24
8
2022
medline:
13
10
2022
entrez:
23
8
2022
Statut:
ppublish
Résumé
Vascular endothelial growth factor A (VEGF-A) and its receptors (VEGFR1 and R2) play important roles in the progression of malignant melanoma through tumor angiogenesis. However, it is not clear whether the VEGF-A/VEGFR1 signaling pathway is involved in the proliferation and migration of melanoma cells. Thus, the effect of VEGF-A on cell migration was investigated in human melanoma cell lines. Of several splicing variants of VEGF-A, VEGF
Identifiants
pubmed: 35997849
doi: 10.1007/s11626-022-00717-3
pii: 10.1007/s11626-022-00717-3
pmc: PMC9550759
doi:
Substances chimiques
Antibodies, Neutralizing
0
Oligonucleotides, Antisense
0
Phosphatidylinositols
0
Vascular Endothelial Growth Factor A
0
Phosphatidylinositol 3-Kinase
EC 2.7.1.137
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Wortmannin
XVA4O219QW
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
758-770Subventions
Organisme : Grants-in-Aid for Scientific Research (C) from the Japanese Ministry of Education, Culture, Sports, Science and Technology
ID : 24593033
Organisme : Grants-in-Aid for Scientific Research (B) from the Japanese Ministry of Education, Culture, Sports, Science and Technology
ID : 18H03000
Informations de copyright
© 2022. The Author(s).
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