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In the present study, we investigated whether treatment with cepharanthine,a biscoclaurine alkaloid extracted from Stephania cepharantha improves the responseto radiotherapy in the oral squamous cell carcinoma (OSCC) cell lines, HSC2, HSC3and HSC4. We examined the potential mechanisms that may contribute to the enhancedradiation response induced by cepharanthine. Growth inhibition was observed in vitrowith radiation or cepharanthine. A co-operative anti-proliferative effect wasobtained when cancer cells were treated with cepharanthine followed by radiation.Cepharanthine also promoted the mitotic death of 3 cell lines by radiation. Theresults from DNA damage repair analysis in the cultured OSCC cells demonstratedthat cepharanthine had a strong inhibitory effect on DNA double-strand break (DSB)repair after radiation. The combined treatment of cepharanthine and radiationled to an increase in the sub-G1 peak as shown by flow cytometry, and markedlyinduced apoptosis through the activation of caspase-3. Tumor xenograft studiesdemonstrated that the combination of cepharanthine and radiation caused growthinhibition and tumor regression of OSCC tumors in athymic mice; tumor volume wasreduced from 765.7 to 226.3 mm3 in HSC2 cells (p&lt;0.01), 391.6 to 43.7 mm3 inHSC3 (p&lt;0.01), and from 572.6 to 174.2 mm3 in HSC4 cells (p&lt;0.01). In addition,combined therapy markedly increased tumor cell apoptosis. Overall, we concludethat cepharanthine enhances tumor radioresponse by multiple mechanisms that mayinvolve the induction of apoptosis and the inhibition of DNA DSB repair afterexposure to radiation.

international journal of oncology

The enhancement of tumor radioresponse by combined treatment with cepharanthine is accompanied by the inhibition of DNA damage repair and the induction of apoptosis in oral squamous cell carcinoma