Cucurbitacin B causes increased radiation sensitivity of human breast cancer cells via G2/M cell cycle arrest

• Main Authors: Duangmano,S., Sae-Lim,P., Suksamrarn,A., Patmasiriwat,P., Domann,F.E.
• Format: Article
• Published: Hindawi Publishing Corporation 2015
• Subjects: Oncology
• Online Access: http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84862280414&origin=inward; http://cmuir.cmu.ac.th/handle/6653943832/38103
• Institution: Chiang Mai University

Purpose. To explore the effects of cucurbitacin B on the radiation survival of human breast cancer cells and to elucidate the cellular mechanism of radiosensitization if any. Materials and Methods. Human breast carcinoma cell lines were treated with cucurbitacin B before irradiation with 0-10Gy of 137Cs gamma rays. The effect of cucurbitacin B on cell-survival following irradiation was evaluated by colony-forming assay. Cell cycle distributions were investigated using flow cytometry. Real-time PCR and western blots were performed to investigate the expression of cell cycle checkpoints. Results. Cucurbitacin B inhibited breast cancer cell proliferation in a dose-dependent manner. Only MDA-MB-231 and MCF7:5C cells but not SKBR-3 cells were radiosensitized by cucurbitacin B. Flow cytometric analysis for DNA content indicated that cucurbitacin B resulted in G2/M arrest in MDA-MB-231 and MCF7:5C but not SKBR-3 cells. Moreover, Real-time PCR and western blot analysis demonstrated upregulated p21 expression before irradiation, a likely cause of the cell cycle arrest. Conclusion. Taken together, these findings suggest that cucurbitacin B causes radiosensitization of some breast cancer cells, and that cucurbitacin B induced G2/M arrest is an important mechanism. Therefore, combinations of cucurbitacin B with radiotherapy may be appropriate for experimental breast cancer treatment. Copyright © 2012 Suwit Duangmano et al.