Apigenin induces apoptosis and impairs head and neck carcinomas EGFR/ErbB2 signaling
Laura Masuelli1, Laura Marzocchella, Alessandro Quaranta
1Department of Experimental Medicine, University of Rome, Sapienza, Rome, Italy.
Abstract:
The development of head and neck squamous cell carcinomas (HNSCCs) is a multistep process progressing from precancerous lesions to highly malignant tumors. A critical role in HNSCCs development and progression is played by EGFR family members including EGFR and ErbB2. The aim of this study was to investigate the effect of apigenin, a low molecular weight flavonoid contained in fruits and vegetables, on growth and survival and on EGFR/ErbB2 signaling in cell lines derived from HNSCCs of the tongue (CAL-27, SCC-15) or pharynx (FaDu). Using sulforhodamine B assay, FACS analysis and activated caspase-3 detection by immunofluorescence, we here demonstrate that apigenin dose-dependently inhibits survival and induces apoptosis of HNSCC cells. Further, by performing western blotting with antibodies specific for phosphorylated EGFR, ErbB2, Erk1/2 and Akt we demonstrate that apigenin reduces ligand-induced phosphorylation of EGFR and ErbB2 and impairs their downstream signaling. On the whole, our results suggest that apigenin properties might be exploited for chemoprevention and/or therapy of head and neck carcinomas.
Insights
Apigenin, a plant flavonoid, effectively inhibits head and neck squamous cell carcinoma (HNSCC) growth and survival. It targets EGFR/ErbB2 signaling pathways, showing potential for HNSCC chemoprevention and therapy.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Head and neck squamous cell carcinomas (HNSCCs) develop through a multistep process.
- Epidermal Growth Factor Receptor (EGFR) family members, including EGFR and ErbB2, are critical in HNSCC development and progression.
Purpose of the Study:
- To investigate the effects of apigenin on HNSCC cell growth, survival, and EGFR/ErbB2 signaling.
- To evaluate apigenin's potential in HNSCC chemoprevention and therapy.
Main Methods:
- Utilized sulforhodamine B assay, FACS analysis, and immunofluorescence for apoptosis detection.
- Performed Western blotting to analyze EGFR, ErbB2, Erk1/2, and Akt phosphorylation.
- Tested apigenin on tongue (CAL-27, SCC-15) and pharynx (FaDu) HNSCC cell lines.
Main Results:
- Apigenin demonstrated dose-dependent inhibition of HNSCC cell survival and induction of apoptosis.
- Apigenin reduced ligand-induced phosphorylation of EGFR and ErbB2.
- Impaired downstream signaling pathways, including Erk1/2 and Akt, were observed.
Conclusions:
- Apigenin exhibits significant anti-cancer properties against HNSCC cells.
- Apigenin's ability to modulate EGFR/ErbB2 signaling suggests its therapeutic potential.
- Further research into apigenin for HNSCC chemoprevention and treatment is warranted.
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