Naringenin inhibits prostate cancer metastasis by blocking voltage-gated sodium channels - 25/08/18
, Tuba AkgunBienvenue sur EM-consulte, la référence des professionnels de santé.
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Graphical abstract |
Highlights |
• | High concentrations of naringenin (75 μM) inhibited the cell proliferation. |
• | Naringenin decreased the movement of MAT-LyLu cells at low concentrations (5–10 μM). |
• | Naringenin (10μM), suppresses the mRNA expression of SCN9A gene. |
• | Naringenin blocks directly or indirectly VGSC encoded by the SCN9A in prostate cancer. |
Abstract |
In this study, we investigated the potential effects of naringenin on the motility of MAT-LyLu cells, which overexpress voltage-gated sodium channels and whose metastatic behaviours are associated with these channels. We first determined the concentration of naringenin that did not show toxic effects or block cell growth. Then, the effects of naringenin on cell motility in the lateral and vertical directions were tested by wound healing assays and transwell invasion assays, respectively. Finally, to determine the suppressive effects of naringenin on cell movement in both directions, the expression of the SCN9A gene, which encodes Nav1.7 voltage-gated sodium channel, was determined by real-time quantitative polymerase chain reaction. The data revealed that high concentrations of naringenin (75 μM) inhibited cell proliferation, whereas low concentrations (5 and 10 μM) decreased the movement of MAT-LyLu cells. Moreover, 10 μM naringenin displayed inhibitory effects on cell movement by reducing the expression of the SCN9A gene at the mRNA level. In conclusion, naringenin was found to have direct or indirect blocking activity on voltage-gated sodium channels encoded by the SCN9A gene.
Le texte complet de cet article est disponible en PDF.Keywords : Naringenin, Voltage-gated sodium channels, Metastasis, Prostate cancer, MAT-LyLu cells, SCN9A
Plan
Vol 106
P. 770-775 - octobre 2018 Retour au numéro
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