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Parishin A Inhibits Oral Squamous Cell Carcinoma via the AKT/mTOR Signaling Pathway
Lei Ma1, Zhibin Liu1, Eungyung Kim2
1Department of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Daegu 37224, Republic of Korea.
Background:
Oral squamous cell carcinoma (OSCC) is an aggressive cancer with limited treatment options. Parishin A, a natural compound derived from Gastrodia elata, possesses multiple therapeutic properties. However, its effects on OSCC remain unexplored.
Purpose:
This study explores the anti-cancer potential of Parishin A on OSCC and its mechanisms.
Methods:
OSCC cell lines YD-10B and Ca9-22 were treated with varying Parishin A concentrations. Cell viability was detected using the CCK-8 assay, and colony formation was evaluated in agarose gel. Migration and invasion ability were assessed through wound healing and Matrigel invasion assays. The protein expression levels involved in the PI3K/AKT/mTOR signaling pathway and epithelial-mesenchymal transition (EMT) markers were examined via Western blotting.
Results:
Parishin A inhibited OSCC cell viability in both dose- and time-dependent manners, with significant reductions at 20, 40, 60, and 80 μM, without affecting normal human gingival fibroblasts. Colony formation decreased substantially at ≥40 μM higher Parishin A concentrations in a dose-dependent manner. Also, migration and invasion assays showed significant suppression by Parishin A treatment concentration ≥40 μM in a dose-dependent manner, as evidenced by decreased wound closure and invasion. Western blot analyses revealed increased E-cadherin levels and decreased N-cadherin and vimentin levels, suggesting EMT inhibition. Parishin A also decreased the phosphorylation levels of PI3K, AKT, and mTOR.
Conclusion:
Collectively, these findings support the potential of Parishin A as an anti-OSCC agent.
Insights
Parishin A, a natural compound, effectively inhibits oral squamous cell carcinoma (OSCC) growth, migration, and invasion. This study highlights Parishin A
Area of Science:
- Oncology
- Natural Products Chemistry
- Molecular Biology
Background:
- Oral squamous cell carcinoma (OSCC) presents a significant therapeutic challenge due to its aggressive nature and limited treatment options.
- Parishin A, a compound from *Gastrodia elata*, exhibits diverse therapeutic properties, but its role in OSCC is not yet understood.
Purpose of the Study:
- To investigate the anti-cancer effects of Parishin A on OSCC.
- To elucidate the underlying molecular mechanisms of Parishin A's action in OSCC.
Main Methods:
- OSCC cell lines were treated with varying concentrations of Parishin A.
- Cell viability, colony formation, migration, and invasion were assessed using CCK-8, agarose gel, wound healing, and Matrigel assays, respectively.
- Protein expression of the PI3K/AKT/mTOR pathway and epithelial-mesenchymal transition (EMT) markers was analyzed by Western blotting.
Main Results:
- Parishin A significantly inhibited OSCC cell viability, colony formation, migration, and invasion in a dose-dependent manner, without affecting normal cells.
- Parishin A treatment led to increased E-cadherin and decreased N-cadherin and vimentin, indicating inhibition of EMT.
- The compound reduced phosphorylation of PI3K, AKT, and mTOR, suggesting modulation of this critical signaling pathway.
Conclusions:
- Parishin A demonstrates potent anti-cancer activity against OSCC.
- These findings suggest Parishin A holds promise as a potential therapeutic agent for oral squamous cell carcinoma.
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