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

Abstract 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 cell...

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Autores principales:	Palacios-Moreno,Juan, Rubio,Cecilia, Quilhot,Wanda, Cavieres,M. Fernanda, Peña,Eduardo de la, Quiñones,Natalia V., Díaz,Hugo, Carrión,Flavio, Henríquez-Roldán,Carlos F., Weinstein-Oppenheimer,Caroline R.
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2019
Materias:	Epanorin Cancer Cytotoxicity Mutagenesis Cell cycle Apoptosis
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100251
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spelling	oai:scielo:S0716-976020190001002512019-12-02Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cellsPalacios-Moreno,JuanRubio,CeciliaQuilhot,WandaCavieres,M. FernandaPeña,Eduardo de laQuiñones,Natalia V.Díaz,HugoCarrión,FlavioHenríquez-Roldán,Carlos F.Weinstein-Oppenheimer,Caroline R. Epanorin Cancer Cytotoxicity Mutagenesis Cell cycle Apoptosis Abstract 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.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.52 20192019-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100251en10.1186/s40659-019-0261-4
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Epanorin Cancer Cytotoxicity Mutagenesis Cell cycle Apoptosis
spellingShingle	Epanorin Cancer Cytotoxicity Mutagenesis Cell cycle Apoptosis Palacios-Moreno,Juan Rubio,Cecilia Quilhot,Wanda Cavieres,M. Fernanda Peña,Eduardo de la Quiñones,Natalia V. Díaz,Hugo Carrión,Flavio Henríquez-Roldán,Carlos F. Weinstein-Oppenheimer,Caroline R. Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells
description	Abstract 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.
author	Palacios-Moreno,Juan Rubio,Cecilia Quilhot,Wanda Cavieres,M. Fernanda Peña,Eduardo de la Quiñones,Natalia V. Díaz,Hugo Carrión,Flavio Henríquez-Roldán,Carlos F. Weinstein-Oppenheimer,Caroline R.
author_facet	Palacios-Moreno,Juan Rubio,Cecilia Quilhot,Wanda Cavieres,M. Fernanda Peña,Eduardo de la Quiñones,Natalia V. Díaz,Hugo Carrión,Flavio Henríquez-Roldán,Carlos F. Weinstein-Oppenheimer,Caroline R.
author_sort	Palacios-Moreno,Juan
title	Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells
title_short	Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells
title_full	Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells
title_fullStr	Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells
title_full_unstemmed	Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells
title_sort	epanorin, a lichen secondary metabolite, inhibits proliferation of mcf-7 breast cancer cells
publisher	Sociedad de Biología de Chile
publishDate	2019
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100251
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Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells

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