Wang Dapeng, Zhang Ke Fen, Du Gang, Wang Jun, Zhao Jinmin
Research Centre for Regenerative Medicine, Guangxi Key Laboratory of Regenerative Medicine, The First Affiliated Hospital of Guangxi Medical University, 530022 Guangxi, Taian, Shandong, China.
Department of Pathology, Taishan Sanatorium, Taian, Shandong, China.
J Cancer Res Ther. 2020;16(2):215-221. doi: 10.4103/jcrt.JCRT_293_19.
Osteosarcoma is a malignant bone tumor and is generally treated with radiotherapy combined with radiosensitizers. The aim of the present study was to investigate the radiosensitization effects of berberine on osteosarcoma cells and the role of Rad51 in radiosensitivity by berberine.
Cells from the human osteosarcoma cell line MG-63 were exposed to γ-ray irradiation (0, 2, 4, 6, and 8 Gy) and berberine (20 μM). Radiosensitivity was evaluated by determining cell viability using an MTT assay. Flow cytometry was used to determine cell cycle and apoptosis. Real-time PCR and western blot were performed to analyze the mRNA and protein expressions of Rad51. The protein levels of E-cadherin and vimentin were also measured to evaluate the epithelial-mesenchymal transition (EMT) process. Tumor invasion was determined by the Boyden chamber assay.
Berberine exacerbated the decline in viability of MG-63 cells exposed to γ-rays irradiation at various concentrations (25, 50, 75, and 100 μmol/L) and induced cell cycle arrest in the G2/M phase as well as apoptosis. The mRNA and protein expressions of Rad51 were significantly decreased by berberine in MG-63 cells. Inhibition of Rad51 by B02 enhanced the radiosensitivity of MG-63 cells. Berberine inhibited their invasive capability as well as increased E-cadherin and decreased vimentin protein levels; this indicated that berberine suppressed the EMT process in MG-63 cells exposed to γ-rays irradiation.
Berberine enhances the radiosensitivity of MG-63 osteosarcoma cells. Rad51 is a potential target of berberine in the radiosensitization of osteosarcoma.
骨肉瘤是一种恶性骨肿瘤，通常采用放疗联合放射增敏剂进行治疗。本研究旨在探讨小檗碱对骨肉瘤细胞的放射增敏作用以及Rad51在小檗碱放射敏感性中的作用。
将人骨肉瘤细胞系MG-63细胞暴露于γ射线照射（0、2、4、6和8 Gy）及小檗碱（20 μM）。采用MTT法测定细胞活力以评估放射敏感性。流式细胞术用于测定细胞周期和凋亡。进行实时PCR和蛋白质印迹分析以检测Rad51的mRNA和蛋白表达。还检测了E-钙黏蛋白和波形蛋白的蛋白水平以评估上皮-间质转化（EMT）过程。通过Boyden小室试验测定肿瘤侵袭能力。
小檗碱在不同浓度（25、50、75和100 μmol/L）下加剧了γ射线照射的MG-63细胞活力的下降，并诱导细胞周期停滞于G2/M期以及凋亡。小檗碱显著降低了MG-63细胞中Rad51的mRNA和蛋白表达。B02对Rad51的抑制增强了MG-63细胞的放射敏感性。小檗碱抑制了它们的侵袭能力，同时增加了E-钙黏蛋白并降低了波形蛋白的蛋白水平；这表明小檗碱抑制了γ射线照射的MG-63细胞中的EMT过程。
小檗碱增强了MG-63骨肉瘤细胞的放射敏感性。Rad51是小檗碱在骨肉瘤放射增敏中的潜在靶点。
