11- epi -Sinulariolide Acetate-induced Apoptosis in Oral Cancer Cells Is Regulated by FOXO Through Inhibition of PI3K/AKT Pathway.

Autor:	Chang TS; Department of Otolaryngology-Head and Neck Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, R.O.C.; School of Medicine, National Defense Medical Center, Taipei, Taiwan, R.O.C.; Institute of Public Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan, R.O.C., Lin JJ; Yu Jun Biotechnology Co., Ltd., Kaohsiung, Taiwan, R.O.C., Cheng KC; Department of Ophthalmology, Kaohsiung Municipal Siaogang Hospital, Kaohsiung, Taiwan, R.O.C.; Department of Ophthalmology, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan, R.O.C.; Department of Ophthalmology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, R.O.C., Su JH; National Museum of Marine Biology and Aquarium, Pingtung, Taiwan, R.O.C., She YY; Department of Otolaryngology-Head and Neck Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, R.O.C., Wu YJ; Yu Jun Biotechnology Co., Ltd., Kaohsiung, Taiwan, R.O.C.; Department of Food and Nutrition, Meiho University, Pingtung, Taiwan, R.O.C.; x00002180@meiho.edu.tw
Jazyk:	angličtina
Zdroj:	Anticancer research [Anticancer Res] 2023 Jun; Vol. 43 (6), pp. 2625-2634.
DOI:	10.21873/anticanres.16429
Abstrakt:	Background/aim: Oral cancer is a general term for carcinomas that occur around the oral tissues, and most are squamous cell carcinoma. Oral cancer is a common disease among Taiwanese males and poses a great threat to national health owing to its high mortality rate. In this study, we used the CAL-27 oral cancer cell lines as in vitro models to investigate the pathways involved in 11-epi-sinulariolide acetate (11-epi-SA)-induced apoptosis. Materials and Methods: There have been no previous studies of the anticancer activity of 11-epi-SA isolated from Sinularia flexibilis against oral cancer. We used MTT assay, cell morphologic analysis, DNA fragmentation, TUNEL/DAPI assay, and JC-1 fluorescence staining to analyze the inhibitory effect of 11-epi-SA against the CAL-27 oral cancer cell line and assessed the potential molecular mechanism of apoptosis using western blot. Results: Our results showed that 11-epi-SA inhibited CAL-27 cell proliferation, and its effect on cell growth was mediated through an apoptotic pathway mechanism. 11-epi-SA inhibited the PI3K/AKT pathway, allowing downstream FOXO to separate from 14-3-3 and return to the nucleus. We also observed that 11-epi-SA disrupted mitochondrial Bcl family protein homeostasis and activated caspase-3 and caspase-9, which led to apoptosis. Conclusion: A low concentration of 11-epi-SA can effectively induce apoptosis in oral cancer cells through the PI3K/AKT/FOXO pathway. 11-epi-SA has great potential as a new drug for the treatment of oral cancer. (Copyright © 2023 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
Databáze:	MEDLINE
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