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The lichen secondary metabolite atranorin suppresses lung cancer cell motility and tumorigenesis
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Journal Article
The lichen secondary metabolite atranorin suppresses lung cancer cell motility and tumorigenesis
2017
Overview
Lichens are symbiotic organisms that produce various secondary metabolites. Here, different lichen extracts were examined to identify secondary metabolites with anti-migratory activity against human lung cancer cells.
Everniastrum vexans
had the most potent inhibitory activity, and atranorin was identified as an active subcomponent of this extract. Atranorin suppressed β-catenin-mediated TOPFLASH activity by inhibiting the nuclear import of β-catenin and downregulating β-catenin/LEF and c-jun/AP-1 downstream target genes such as CD44, cyclin-D1 and c-myc. Atranorin decreased KAI1 C-terminal interacting tetraspanin (KITENIN)-mediated AP-1 activity and the activity of the KITENIN 3′-untranslated region. The nuclear distribution of the AP-1 transcriptional factor, including c-jun and c-fos, was suppressed in atranorin-treated cells, and atranorin inhibited the activity of Rho GTPases including Rac1, Cdc42, and RhoA, whereas it had no effect on epithelial-mesenchymal transition markers. STAT-luciferase activity and nuclear STAT levels were decreased, whereas total STAT levels were moderately reduced. The human cell motility and lung cancer RT² Profiler PCR Arrays identified additional atranorin target genes. Atranorin significantly inhibited tumorigenesis
in vitro
and
in vivo
. Taken together, our results indicated that
E. vexans
and its subcomponent atranorin may inhibit lung cancer cell motility and tumorigenesis by affecting AP-1, Wnt, and STAT signaling and suppressing RhoGTPase activity.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 38/39
/ 38/77
/ 64/60
/ 82/83
/ 96/1
/ 96/109
/ 96/63
/ 96/95
/ Antineoplastic Agents - chemistry
/ Antineoplastic Agents - pharmacology
/ Biological Products - chemistry
/ Biological Products - pharmacology
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Cell Transformation, Neoplastic - drug effects
/ Gene Expression Regulation, Neoplastic
/ Humanities and Social Sciences
/ Humans
/ Hydroxybenzoates - chemistry
/ Hydroxybenzoates - metabolism
/ Hydroxybenzoates - pharmacology
/ Lichens
/ Motility
/ Proto-Oncogene Proteins c-jun - metabolism
/ rho GTP-Binding Proteins - metabolism
/ Science
/ Signal Transduction - drug effects
