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Published on: March 17, 2018
Apigenin impairs oral squamous cell carcinoma growth in vitro inducing cell cycle arrest and apoptosis
Daniele Maggioni1, Werner Garavello, Roberta Rigolio
1Department of Surgery and Translational Medicine, University of Milan-Bicocca, I-20900 Monza, Italy.
Abstract:
In the present study, we investigated the effect of apigenin, a flavonoid widely present in fruits and vegetables, on a tongue oral cancer-derived cell line (SCC-25) and on a keratinocyte cell line (HaCaT), with the aim of unveiling its antiproliferative mechanisms. The effect of apigenin on cell growth was evaluated by MTT assay, while apoptosis was investigated by phosphatidyl serine membrane translocation and cell cycle distribution by propidium iodide DNA staining through flow cytometry. In addition the expression of cyclins and cyclin-dependent kinases was evaluated by western blotting. A reduction of apigenin-induced cell growth was found in both cell lines, although SCC-25 cells were significantly more sensitive than the immortalized keratinocytes, HaCaT. Moreover, apigenin induced apoptosis and modulated the cell cycle in SCC-25 cells. Apigenin treatment resulted in cell cycle arrest at both G0/G1 and G2/M checkpoints, while western blot analysis revealed the decreased expression of cyclin D1 and E, and inactivation of CDK1 upon apigenin treatment. These results demonstrate the anticancer potential of apigenin in an oral squamous cell carcinoma cell line, suggesting that it may be a very promising chemopreventive agent due to its cancer cell cytotoxic activity and its ability to act as a cell cycle modulating agent at multiple levels.
Insights
Apigenin, a plant flavonoid, shows anticancer potential against oral cancer cells (SCC-25) by reducing growth and inducing apoptosis. It effectively modulates the cell cycle, suggesting promise as a chemopreventive agent.
Area of Science:
- Phytochemistry
- Molecular Biology
- Cancer Research
Background:
- Flavonoids, like apigenin found in fruits and vegetables, are studied for their health benefits.
- Oral squamous cell carcinoma (OSCC) is a significant global health concern requiring novel therapeutic strategies.
Purpose of the Study:
- To investigate the antiproliferative mechanisms of apigenin in an oral cancer cell line (SCC-25) and a keratinocyte cell line (HaCaT).
- To evaluate apigenin's potential as an anticancer and chemopreventive agent.
Main Methods:
- Cell viability assessed using MTT assay.
- Apoptosis evaluated via phosphatidyl serine membrane translocation.
- Cell cycle distribution analyzed by flow cytometry using propidium iodide staining.
- Expression of cyclins and cyclin-dependent kinases (CDKs) determined by western blotting.
Main Results:
- Apigenin reduced cell growth in both SCC-25 and HaCaT cells, with SCC-25 cells showing higher sensitivity.
- Apigenin induced apoptosis and modulated the cell cycle in SCC-25 cells.
- Cell cycle arrest occurred at G0/G1 and G2/M checkpoints, with decreased cyclin D1/E expression and CDK1 inactivation.
Conclusions:
- Apigenin exhibits significant anticancer potential against oral squamous cell carcinoma cells.
- Apigenin acts as a cell cycle modulating agent at multiple levels, supporting its role as a chemopreventive agent.
- Further research into apigenin's therapeutic applications in oral cancer is warranted.
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