Su, C.-C.; Yu, C.-C.; Shih, Y.-W.; Liu, K.-L.; Chen, H.-W.; Wu, C.-C.; Yang, Y.-C.; Yeh, E.-L.; Li, C.-C. Protective Effect of Alpha-Linolenic Acid on Human Oral Squamous Cell Carcinoma Metastasis and Apoptotic Cell Death. Nutrients2023, 15, 4992.
Su, C.-C.; Yu, C.-C.; Shih, Y.-W.; Liu, K.-L.; Chen, H.-W.; Wu, C.-C.; Yang, Y.-C.; Yeh, E.-L.; Li, C.-C. Protective Effect of Alpha-Linolenic Acid on Human Oral Squamous Cell Carcinoma Metastasis and Apoptotic Cell Death. Nutrients 2023, 15, 4992.
Su, C.-C.; Yu, C.-C.; Shih, Y.-W.; Liu, K.-L.; Chen, H.-W.; Wu, C.-C.; Yang, Y.-C.; Yeh, E.-L.; Li, C.-C. Protective Effect of Alpha-Linolenic Acid on Human Oral Squamous Cell Carcinoma Metastasis and Apoptotic Cell Death. Nutrients2023, 15, 4992.
Su, C.-C.; Yu, C.-C.; Shih, Y.-W.; Liu, K.-L.; Chen, H.-W.; Wu, C.-C.; Yang, Y.-C.; Yeh, E.-L.; Li, C.-C. Protective Effect of Alpha-Linolenic Acid on Human Oral Squamous Cell Carcinoma Metastasis and Apoptotic Cell Death. Nutrients 2023, 15, 4992.
Abstract
Oral cancer ranks sixth among Taiwan's top 10 cancers, and most patients with poor prognosis acquire metastases. The essential fatty acid alpha-linolenic acid (ALA) has been found to diminish many cancer properties. However, the anti-cancer activity of ALA in oral cancer has yet to be determined. Migration and invasion assays confirmed OSCC cells' EMT capabilities, whereas flow cytometry and Western blotting identified the molecular pathways. ALA dramatically reduced cell growth in a concentration dependent manner, according to the findings. Low concentrations of ALA (100 or 200 μM) inhibit colony formation, expression of Twist and EMT-related proteins, expression of MMP2/-9 proteins and enzyme activity, as well as cell migration and invasion. Treatment with high concentrations of ALA (200 or 400 μM) greatly increases JNK phosphorylation and c-jun nuclear accumulation, then upregulates the FasL/caspase8/caspase3 and Bid/cytochrome c/caspase9/caspase3 pathways, leading to cell death. Low concentrations of ALA inhibit SAS and GNM cell migration and invasion by suppressing Twist and downregulating EMT-related proteins, or by decreasing the protein expression and enzyme activity of MMP-2/-9, whereas high concentrations of ALA promote apoptosis by activating the JNK/FasL/caspase 8/caspase 3-extrinsic pathway and the Bid/cytochrome c/caspase 9 pathway. ALA demonstrates potential as a treatment for OSCC patients.
Medicine and Pharmacology, Oncology and Oncogenics
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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