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Updated: Feb 8, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Naringenin inhibits prostate cancer metastasis by blocking voltage-gated sodium channels
Hatice Gumushan Aktas1, Tuba Akgun1
1Biology Department, Faculty of Arts & Sciences, Harran University, Osmanbey Campus, Sanliurfa, Turkey.
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.
Insights
Naringenin, a natural compound, was found to reduce the movement of MAT-LyLu cancer cells. It achieves this by decreasing the expression of the SCN9A gene, which encodes a key sodium channel involved in cell metastasis.
Area of Science:
- Biochemistry
- Molecular Biology
- Cancer Research
Background:
- MAT-LyLu cells exhibit metastatic behavior linked to overexpression of voltage-gated sodium channels.
- Understanding the role of these channels in cell motility is crucial for developing anti-metastatic strategies.
Purpose of the Study:
- To investigate the effects of naringenin on MAT-LyLu cell motility.
- To determine if naringenin affects the expression of the SCN9A gene, which encodes the Nav1.7 sodium channel.
Main Methods:
- Cell proliferation and toxicity assays were performed to establish non-toxic naringenin concentrations.
- Wound healing and transwell invasion assays assessed naringenin's impact on lateral and vertical cell motility.
- Real-time quantitative polymerase chain reaction (RT-qPCR) measured SCN9A gene expression.
Main Results:
- Naringenin at high concentrations (75 μM) inhibited cell proliferation.
- Low concentrations of naringenin (5 and 10 μM) significantly decreased MAT-LyLu cell movement.
- 10 μM naringenin reduced SCN9A gene expression at the mRNA level, correlating with decreased cell motility.
Conclusions:
- Naringenin exhibits anti-motility effects on MAT-LyLu cells.
- These effects are associated with the suppression of SCN9A gene expression.
- Naringenin may act by directly or indirectly blocking voltage-gated sodium channels encoded by SCN9A.
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