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Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells.
Biological Research ( IF 4.3 ) Pub Date : 2019-10-10 , DOI: 10.1186/s40659-019-0261-4
Juan Palacios-Moreno 1 , Cecilia Rubio 1 , Wanda Quilhot 1 , M Fernanda Cavieres 1, 2 , Eduardo de la Peña 3 , Natalia V Quiñones 1, 2 , Hugo Díaz 4 , Flavio Carrión 5 , Carlos F Henríquez-Roldán 6 , Caroline R Weinstein-Oppenheimer 1, 2
Affiliation  

BACKGROUND Epanorin (EP) is a secondary metabolite of the Acarospora lichenic species. EP has been found in lichenic extracts with antimicrobial activity, and UV-absorption properties have been described for closely related molecules; however, its antiproliferative activity in cancer cells has not yet been explored. It has been hypothesized that EP inhibits cancer cell growth. MCF-7 breast cancer cells, normal fibroblasts, and the non-transformed HEK-293 cell line were exposed to increasing concentrations of EP, and proliferation was assessed by the sulforhodamine-B assay. RESULTS MCF-7 cells exposed to EP were examined for cell cycle progression using flow cytometry, and DNA fragmentation was examined using the TUNEL assay. In addition, EP's mutagenic activity was assessed using the Salmonella typhimurium reverse mutation assay. The data showed that EP inhibits proliferation of MCF-7 cells, and it induces cell cycle arrest in G0/G1 through a DNA fragmentation-independent mechanism. Furthermore, EP's lack of overt cytotoxicity in the normal cell line HEK-293 and human fibroblasts in cell culture is supported by the absence of mutagenic activity of EP. CONCLUSION EP emerges as a suitable molecule for further studies as a potential antineoplastic agent.

中文翻译:

Epanorin是一种地衣的次生代谢产物,可抑制MCF-7乳腺癌细胞的增殖。

背景技术Epanorin(EP)是Acarospora地衣种的次生代谢产物。已在具有抗菌活性的地衣提取物中发现了EP,并且已描述了与紧密相关的分子的紫外线吸收特性。但是,尚未探索其在癌细胞中的抗增殖活性。据推测,EP抑制癌细胞的生长。将MCF-7乳腺癌细胞,正常成纤维细胞和未转化的HEK-293细胞系暴露于浓度不断提高的EP中,并通过磺基罗丹明B检测评估增殖。结果使用流式细胞仪检测了暴露于EP的MCF-7细胞的细胞周期进程,并使用TUNEL法检测了DNA片段化。此外,使用鼠伤寒沙门氏菌反向突变试验评估了EP的诱变活性。数据显示,EP抑制MCF-7细胞的增殖,并通过不依赖DNA片段化的机制诱导G0 / G1细胞周期停滞。此外,EP在细胞培养中在正常细胞系HEK-293和人成纤维细胞中缺乏明显的细胞毒性,这归因于EP缺乏诱变活性。结论EP作为一种潜在的抗肿瘤药物出现了作为进一步研究的合适分子。
更新日期:2020-04-22
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