ArticleBiological research2019
Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells.
Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Molecular phylogeny and ecological diversity of endolichenic fungi inhabiting Acarospora schleicheri (Ach.) A. Massal, isolated from a Chilean Andean zone.Scientific reports · 2026Article
- Arctic lichen Cladonia borealis-induced cell death is mediated by p53-independent activation of Caspase-9 and PARP-1 signaling in human colorectal cancer cell lines.Journal of microbiology (Seoul, Korea) · 2025Article
- Review
- The metabolite 5-methyl-1,3-benzenediol and its derivative methyl-2,4-dihydroxy-6-methylbenzoate from the lichen3 Biotech · 2021Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundEpanorin (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.
resultsMCF-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.
conclusionEP emerges as a suitable molecule for further studies as a potential antineoplastic agent.
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