ArticlePharmaceuticals (Basel, Switzerland)2024
Parishin A Inhibits Oral Squamous Cell Carcinoma via the AKT/mTOR Signaling Pathway.
Article in Pharmaceuticals (Basel, Switzerland), 2024. 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.
- Vemurafenib Induces Apoptosis via JNK Activation and AKT Inhibition in Hepatocellular Carcinoma.Journal of Cancer · 2026Article
- Unraveling the metabolic network and key bioactive compound accumulation during critical developmental stages ofFrontiers in plant science · 2026Article
- Sestrin2 Knockdown Impairs Proliferation, Migration, Invasion, and Apoptosis in OSCC Cells via PI3K/AKT/mTOR and MAPK Pathways.Current issues in molecular biology · 2025Article
- Simultaneous Quantification of Multiple Analytes in Rat Plasma by UHPLC-MS/MS Following Oral Administration ofMolecules (Basel, Switzerland) · 2025Article
- Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- MK2-mediated AKT/MYC signaling activation promotes epithelial-mesenchymal transition in lung adenocarcinoma.Frontiers in genetics · 2025Article
- Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers.Oncology research · 2025Review
- Advances in Preventive and Therapeutic Strategies for Oral Cancer: A Short Review.Journal of cancer prevention · 2024Review
- Evolving Therapeutic Strategies in Esophageal Squamous Cell Carcinoma: Advances and Perspectives.Journal of cancer prevention · 2024Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOral squamous cell carcinoma (OSCC) is an aggressive cancer with limited treatment options. Parishin A, a natural compound derived from PURPOSE: This study explores the anti-cancer potential of Parishin A on OSCC and its mechanisms.
methodsOSCC 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.
resultsParishin 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.
conclusionCollectively, these findings support the potential of Parishin A as an anti-OSCC agent.
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