Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells

dc.contributor.authorPalacios-Moreno, Juan
dc.contributor.authorRubio, Cecilia
dc.contributor.authorQuilhot, Wanda
dc.contributor.authorCavieres, M. Fernanda
dc.contributor.authorPeña, Eduardo de la
dc.contributor.authorQuiñones, Natalia V.
dc.contributor.authorDíaz, Hugo
dc.contributor.authorCarrión, Flavio
dc.contributor.authorHenríquez-Roldán, Carlos F.
dc.contributor.authorWeinstein-Oppenheimer, Caroline R.
dc.date.accessioned2020-03-09T17:19:46Z
dc.date.available2020-03-09T17:19:46Z
dc.date.issued2019
dc.description.abstractBackground: 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.
dc.format.extent11 p.
dc.identifier.citationBiological Research 52, 55 (2019).
dc.identifier.urihttp://hdl.handle.net/11447/3130
dc.identifier.urihttp://dx.doi.org/10.1186/s40659-019-0261-4
dc.language.isoen
dc.subjectEpanorin
dc.subjectCancer
dc.subjectCytotoxicity
dc.subjectMutagenesis
dc.subjectCell cycle
dc.subjectApoptosis
dc.titleEpanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells
dc.typeArticle

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