ArticleMolecular medicine reports2016
Inhibitory effects of dieckol on hypoxia-induced epithelial-mesenchymal transition of HT29 human colorectal cancer cells.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular insights into the anticancer properties of dieckol: a comprehensive review.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Phlorotannins: Novel Orally Administrated Bioactive Compounds That Induce Mitochondrial Dysfunction and Oxidative Stress in Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- An electroaffinity labelling platform for chemoproteomic-based target identification.Nature chemistry · 2023Article
- Unveiling the Potential of BenzylethyleneAryl-Urea Scaffolds for the Design of New Onco Immunomodulating Agents.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Dieckol Inhibits Autophagic Flux and Induces Apoptotic Cell Death in A375 Human Melanoma Cells via Lysosomal Dysfunction and Mitochondrial Membrane Impairment.International journal of molecular sciences · 2022Article
- Call the Eckols: Present and Future Potential Cancer Therapies.Marine drugs · 2022Review
- Inhibition of A549 Lung Cancer Cell Migration and Invasion byMarine drugs · 2021Article
- Iron and copper complexes with antioxidant activity as inhibitors of the metastatic potential of glioma cells.RSC advances · 2020Article
- Redox regulation in tumor cell epithelial-mesenchymal transition: molecular basis and therapeutic strategy.Signal transduction and targeted therapyReview
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia-induced epithelial-mesenchymal transition (EMT) has been identified as essential for tumor progression and metastasis. The present study examined the effects of an antioxidant, dieckol, on hypoxia‑induced EMT in HT29 human colorectal cancer cells. HT29 cells were treated with a hypoxia‑inducing agent, CoCl2, and an increase in the levels of intracellular reactive oxygen species (ROS) and various morphological changes, such as loss of cell‑cell contact and aggressive cell migration were observed. CoCl2 also induced an increase in the expression of hypoxia‑inducible factor 1α (HIF1α) and various mesenchymal‑specific markers, including vimentin and snail family transcriptional repressor 1 (Snail1), and a decrease in the expression of E‑cadherin, thus suggesting that CoCl2 induced EMT in HT29 cells. Conversely, the CoCl2‑induced EMT of HT29 cells was suppressed following treatment with dieckol. In addition, ROS generation, EMT marker protein expression and intracellular localization, cell migration and cell invasion were attenuated following dieckol treatment. The findings of the present study suggested that dieckol may inhibit hypoxia‑induced EMT in HT29 cells by regulating the levels of cellular ROS and protein expression levels downstream of the HIF1α signaling pathway. Therefore, dieckol has the potential to become an attractive therapeutic agent for the treatment of colorectal cancer.
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