Journal
SAUDI JOURNAL OF BIOLOGICAL SCIENCES
Volume 28, Issue 9, Pages 4908-4915Publisher
ELSEVIER
DOI: 10.1016/j.sjbs.2021.07.019
Keywords
Dieckol; Osteosarcoma; Cell Proliferation; MG-63 cells; Apoptosis
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The study investigated the in vitro anticancer effects of dieckol on human osteosarcoma cells, showing that dieckol could effectively inhibit cell viability and promote apoptosis by blocking the PI3K/AKT/mTOR signaling pathway. This suggests that dieckol may be a promising candidate for osteosarcoma management in the future.
Background: Osteosarcoma (OS) is the most common malignant bone cancer with more metastasis and increased occurrence in children and teen-agers and being responsible for more number of morbidity and mortality worldwide. Objective: The current exploration was planned study the in vitro anticancer actions of dieckol against human OS MG-63 cells via PI3K/AKT/mTOR signaling inhibition. Methodology: The cytotoxicity of dieckol was scrutinized by MTT assay. Effects of dieckol on the ROS accumulation, apoptotic cell death, and MMP level in the MG-63 cells were studied by respective fluorescence staining assays. The levels of proliferative, inflammatory, and apoptotic markers in the dieckol treated MG-63 cells were scrutinized by marker specific kits. The expressions of PI3K, AKT, and mTOR was assayed by RT-PCR. Results: The MTT assay revealed that the dieckol dose dependently prevented MG-63 cells viability and the IC50 was found at 15 mM. Dieckol treatment effectively reduced the MMP level and improved the ROS generation and apoptosis in MG-63 cells. Dieckol also regulated the proliferative (cyclin D1), inflammatory (COX-2, IL-6, TNF-alpha, and NF-kappa B), and apoptotic (caspase-3, Bax, Bcl-2) markers in the MG-63 cells. The PI3K/AKT/mTOR signaling in the MG-63 cells were effectively inhibited by the dieckol treatment. Conclusion: In conclusion, our findings from this study recommends that the dieckol could be a talented anticancer candidate for the OS management in the future. (C) 2021 The Author(s). Published by Elsevier B.V. on behalf of King Saud University.
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