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首页> 外文期刊>International Journal of Biomedical Science >Methyl Angolensate from Callus of Indian Redwood Induces Cytotoxicity in Human Breast Cancer Cells
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Methyl Angolensate from Callus of Indian Redwood Induces Cytotoxicity in Human Breast Cancer Cells

机译：来自印度红杉愈伤组织的甲基去甲辛酸酯诱导人乳腺癌细胞的细胞毒性

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AIM: Natural products discovered from medicinal plants have played an important role in the treatment of cancer. Methyl angolensate (MA), a tetranortriterpenoid obtained from the root callus of Indian Redwood tree, Soymida febrifuga Roxb. (A.Juss) was tested for its anticancer properties on breast cancer cells.METHODS: Cell viability was tested using trypan blue, MTT and LDH assays. Tritiated thymidine assay and flowcytometry were used to study effect of MA on cell proliferation. The activation of apoptosis was checked by annexin V and JC-1 staining followed by FACS analysis. Immunoblotting analysis was used for studying expression of apoptotic and DNA double strand break repair proteins. RESULTS: We find that MA inhibited the growth of breast cancer cell line, T47D in a time- and dose-dependent manner. MA treatment led to the inhibition of cell proliferation as detected by tritiated thymidine assay and flowcytometry. Further, MA treated cells exhibited typical apoptotic morphological changes and led to the accumulation of subG1 peak in cell cycle distribution. The induction of apoptosis was further confirmed both by annexin V staining and JC1 staining. We also find that MA activates MAP kinase pathway to induce apoptosis. Besides, we find a time dependent activation followed by degradation of DNA double-strand break repair proteins upon treatment with MA. CONCLUSION: These results suggest that MA induces cytotoxicity in breast cancer cells. Further, the altered expression of DSB repair proteins in MA treated cells may control the induction of apoptosis in these cancer cells.
机译：目的：从药用植物中发现的天然产物在癌症治疗中起着重要作用。甲基无花果酸酯（MA），一种四降三萜烯，从印度红木树（Soymida febrifuga Roxb）的根愈伤组织中获得。测试（A.Juss）对乳腺癌细胞的抗癌特性。方法：使用锥虫蓝，MTT和LDH分析测试细胞活力。 ti胸腺嘧啶核苷分析和流式细胞仪用于研究MA对细胞增殖的影响。通过膜联蛋白V和JC-1染色检查细胞凋亡的激活，然后进行FACS分析。免疫印迹分析用于研究凋亡和DNA双链断裂修复蛋白的表达。结果：我们发现MA以时间和剂量依赖性方式抑制乳腺癌细胞T47D的生长。 MA处理导致thy化胸苷测定和流式细胞仪检测到的细胞增殖受到抑制。此外，MA处理的细胞表现出典型的凋亡形态变化，并导致subG1峰在细胞周期分布中积累。膜联蛋白V染色和JC1染色都进一步证实了细胞凋亡的诱导。我们还发现，MA激活MAP激酶途径来诱导细胞凋亡。此外，我们发现了时间依赖性激活，随后在用MA处理后降解了DNA双链断裂修复蛋白。结论：这些结果表明MA可诱导乳腺癌细胞的细胞毒性。此外，在MA处理的细胞中DSB修复蛋白表达的改变可以控制这些癌细胞中凋亡的诱导。

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