Apigenin impairs oral squamous cell carcinoma growth in vitro inducing cell cycle arrest and apoptosis

Daniele Maggioni, Werner Garavello, Roberta Rigolio, Lorenzo Pignataro, Renato Gaini, Gabriella Nicolini

Research output: Contribution to journalArticlepeer-review


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 G 0/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.

Original languageEnglish
Pages (from-to)1675-1682
Number of pages8
JournalInternational Journal of Oncology
Issue number5
Publication statusPublished - Nov 2013


  • Apigenin
  • Cell cycle
  • HaCaT and SCC-25
  • Oral squamous cell carcinoma

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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