2. Academic Validation
  3. Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells

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

  • Biol Res. 2019 Oct 10;52(1):55. 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 7 8
Affiliations

Affiliations

  • 1 Escuela de Química y Farmacia, Facultad de Farmacia, Universidad de Valparaíso, Av. Gran Bretaña 1093, Playa Ancha, CP 2360102, Valparaiso, Chile.
  • 2 Centro de Investigación Farmacopea Chilena, Valparaiso, Chile.
  • 3 ICA-Mutagénesis Ambiental, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
  • 4 Escuela de Ingeniería en Medioambiente, Facultad de Ingeniería, Universidad de Valparaíso, Valparaiso, Chile.
  • 5 Programa de Inmunología Traslacional, Facultad de Medicina, Clínica Alemana, Universidad del Desarrollo, Las Condes, Santiago, Chile.
  • 6 Instituto de Estadística, Facultad de Ciencias, Universidad de Valparaíso, Playa Ancha, Valparaiso, Chile.
  • 7 Escuela de Química y Farmacia, Facultad de Farmacia, Universidad de Valparaíso, Av. Gran Bretaña 1093, Playa Ancha, CP 2360102, Valparaiso, Chile. Caroline.weinstein@uv.cl.
  • 8 Centro de Investigación Farmacopea Chilena, Valparaiso, Chile. Caroline.weinstein@uv.cl.
PMID: 31601259 DOI: 10.1186/s40659-019-0261-4
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.

Keywords

Apoptosis; Cancer; Cell cycle; Cytotoxicity; Epanorin; Mutagenesis.

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