ArticleCancer cell international2017
PI3Kα isoform-dependent activation of RhoA regulates Wnt5a-induced osteosarcoma cell migration.
Article in Cancer cell international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Deciphering lncRNA and circRNA control of autophagy in osteosarcoma mechanisms and clinical translation.Discover oncology · 2026Review
- Identification of epigenetic silencing of the SFRP2 gene in colorectal cancer as a clinical biomarker and molecular significance.Journal of translational medicine · 2024Article
- Overexpression of Wnt5a promoted the protective effect of mesenchymal stem cells on Lipopolysaccharide-induced endothelial cell injury via activating PI3K/AKT signaling pathway.BMC infectious diseases · 2024Article
- Non-canonical WNT5A-ROR signaling: New perspectives on an ancient developmental pathway.Current topics in developmental biology · 2023Article
- Identification of key serum biomarkers for the diagnosis and metastatic prediction of osteosarcoma by analysis of immune cell infiltration.Cancer cell international · 2022Article
- The roles of glycolysis in osteosarcoma.Frontiers in pharmacology · 2022Review
- Rho-GEF Trio regulates osteosarcoma progression and osteogenic differentiation through Rac1 and RhoA.Cell death & disease · 2021Article
- The WNT receptor ROR2 drives the interaction of multiple myeloma cells with the microenvironment through AKT activation.Leukemia · 2020Article
- ROR2 receptor promotes the migration of osteosarcoma cells in response to Wnt5a.Cancer cell international · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe have reported that the phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway mediated Wnt5a-induced osteosarcoma cell migration. However, the signaling pathways regulating Wnt5a/PI3K/Akt-mediated cell migration remains poorly defined in osteosarcoma cells.
methodsWe evaluated the activations of RhoA, Rac1 and Cdc42 in osteosarcoma MG-63 and U2OS cells with small G-protein activation assay. Boyden chamber assays were used to confirm the migration of cells transfected indicated constructs or siRNA specific against RhoA. A panel of inhibitors of PI3K and Akt treated osteosarcoma cells and blocked kinase activity. Western blotting and RhoA activation assay were employed to measure the effect of kinase inhibitors and activations of RhoA and Akt.
resultsWe found that Wnt5a had a potent stimulatory effect on RhoA activation, but not on Rac1 and Cdc42 activations. Wnt5a-induced cell migration was largely abolished by siRNA specific against RhoA. DN-RhoA (GFP-RhoA-N19) was also capable of retarding Wnt5a-induced cell migration, but the overexpression of CA-RhoA (GFP-RhoA-V14) was not able to accelerate cell migration. The Wnt5a-induced activation of RhoA was mostly blocked by pretreatment of LY294002 (PI3K inhibitor) and MK-2206 (Akt inhibitor). Furthermore, we found that the Wnt5a-induced activation of RhoA was mostly blocked by pretreatment of HS-173 (PI3Kα inhibitor). Lastly, the phosphorylation of Akt (p-Ser473) was not altered by transfection with siRNA specific against RhoA or DN-RhoA (GFP-RhoA-N19).
conclusionsTaken together, we demonstrate that RhoA acts as the downstream of PI3K/Akt signaling (specific PI3Kα, Akt1 and Akt2 isoforms) and mediated Wnt5a-induced the migration of osteosarcoma cells.
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