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Corilagin Represses Epithelial to Mesenchymal Transition Process Through Modulating Wnt/β-Catenin Signaling Cascade
Sun Tae Hwang1, Min Hee Yang1,2, Alan Prem Kumar3,4
1Department of Science in Korean Medicine, Kyung Hee University, Seoul 02447, Korea.
Abstract:
Corilagin (CLG), a major component of several medicinal plants, can exhibit diverse pharmacological properties including those of anti-cancer, anti-inflammatory, and hepatoprotective qualities. However, there are no prior studies on its potential impact on the epithelial-to-mesenchymal transition (EMT) process. EMT can lead to dissemination of tumor cells into other organs and promote cancer progression. Hence, we aimed to investigate the effect of CLG on EMT and its mechanism(s) of action in tumor cells. We noted that CLG reduced the expression of various epithelial markers and up-regulated the expression of Occludin and E-cadherin in both basal and TGFβ-stimulated tumor cells. CLG treatment also abrogated cellular invasion and migration in colon and prostate carcinoma cells. In addition, CLG effectively attenuated the Wnt/β-catenin signaling cascade in TGFβ-stimulated cells. Overall, our study suggests that CLG may function as and effective modulator of EMT and metastasis in neoplastic cells.
Insights
Corilagin (CLG) inhibits cancer cell metastasis by modulating the epithelial-to-mesenchymal transition (EMT). This natural compound reduces tumor cell invasion and migration, offering potential as an anti-cancer therapeutic agent.
Area of Science:
- Pharmacology
- Cancer Biology
- Molecular Medicine
Background:
- Corilagin (CLG), a plant-derived compound, possesses known anti-cancer, anti-inflammatory, and hepatoprotective properties.
- The epithelial-to-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cell dissemination and metastasis.
- No previous studies have investigated the impact of Corilagin on EMT.
Purpose of the Study:
- To investigate the effect of Corilagin (CLG) on the epithelial-to-mesenchymal transition (EMT) process in tumor cells.
- To elucidate the underlying mechanisms by which CLG influences EMT and metastasis.
Main Methods:
- Treatment of tumor cells with Corilagin (CLG).
- Analysis of epithelial and mesenchymal marker expression.
- Assessment of cellular invasion and migration assays.
- Investigation of the Wnt/β-catenin signaling pathway.
Main Results:
- Corilagin (CLG) reduced the expression of epithelial markers and increased Occludin and E-cadherin levels.
- CLG treatment significantly abrogated cellular invasion and migration in colon and prostate carcinoma cells.
- CLG attenuated the Wnt/β-catenin signaling cascade in TGFβ-stimulated cells.
Conclusions:
- Corilagin (CLG) demonstrates potential as an inhibitor of EMT and metastasis in neoplastic cells.
- CLG may serve as a valuable therapeutic agent for managing cancer progression and metastasis.
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