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Arctigenin represses TGF-β-induced epithelial mesenchymal transition in human lung cancer cells
Yanrui Xu1, Zhiyuan Lou1, Seong-Ho Lee1
1Department of Nutrition and Food Science, University of Maryland, College Park, MD 20742, USA.
Abstract:
Arctigenin (ARC) is a lignan that is abundant in Asteraceae plants, which show anti-inflammatory and anti-cancer activities. The current study investigated whether ARC affects cancer progression and metastasis, focusing on EMT using invasive human non-small cell lung cancer (NSCLC) cells. No toxicity was observed in the cells treated with different doses of ARC (12-100 μM). The treatment of ARC repressed TGF-β-stimulated changes of metastatic morphology and cell invasion and migration. ARC inhibited TGF-β-induced phosphorylation and transcriptional activity of smad2/3, and expression of snail. ARC also decreased expression of N-cadherin and increased expression of E-cadherin in dose-dependent and time-dependent manners. These changes were accompanied by decreased amount of phospho-smad2/3 in nucleus and nuclear translocation of smad2/3. Moreover, ARC repressed TGF-β-induced phosphorylation of ERK and transcriptional activity of β-catenin. Our data demonstrate anti-metastatic activity of ARC in lung cancer model.
Insights
Arctigenin (ARC) effectively inhibits lung cancer metastasis by suppressing epithelial-mesenchymal transition (EMT) without causing toxicity. This natural compound targets key signaling pathways involved in cancer progression.
Area of Science:
- Phytochemistry
- Cancer Biology
- Molecular Oncology
Background:
- Arctigenin (ARC), a lignan from Asteraceae plants, exhibits known anti-inflammatory and anti-cancer properties.
- Cancer metastasis, particularly in non-small cell lung cancer (NSCLC), remains a significant clinical challenge.
- Epithelial-mesenchymal transition (EMT) is a critical process driving cancer cell invasion and metastasis.
Purpose of the Study:
- To investigate the anti-metastatic effects of Arctigenin (ARC) on invasive human non-small cell lung cancer (NSCLC) cells.
- To elucidate the molecular mechanisms underlying ARC's action, focusing on EMT.
- To assess the safety profile of ARC in NSCLC cells.
Main Methods:
- Treatment of NSCLC cells with varying doses of ARC (12-100 μM).
- Stimulation of cells with Transforming Growth Factor-beta (TGF-β) to induce metastatic phenotypes.
- Analysis of cell morphology, invasion, migration, and expression/phosphorylation of key proteins (smad2/3, snail, N-cadherin, E-cadherin, ERK, β-catenin).
- Assessment of smad2/3 nuclear translocation.
Main Results:
- ARC demonstrated no observable toxicity in NSCLC cells at tested concentrations.
- ARC treatment repressed TGF-β-induced changes in metastatic morphology, invasion, and migration.
- ARC inhibited TGF-β-induced smad2/3 phosphorylation and transcriptional activity, as well as snail expression.
- ARC decreased N-cadherin and increased E-cadherin expression in a dose- and time-dependent manner.
- ARC reduced phospho-smad2/3 levels in the nucleus and its nuclear translocation.
- ARC repressed TGF-β-induced ERK phosphorylation and β-catenin transcriptional activity.
Conclusions:
- Arctigenin exhibits significant anti-metastatic activity in a non-small cell lung cancer model.
- ARC effectively suppresses cancer cell invasion and migration by inhibiting key EMT signaling pathways.
- These findings highlight ARC as a potential therapeutic agent for combating lung cancer metastasis.
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