Experimental study of atorvastatin regulation of HL-60 leukemia cell apoptosis through PI3K/AKT/mTOR

• Main Author: Lin Mei
• Format: Article
• Language: English
• Published: Editorial Board of Journal of Hainan Medical University 2016-03-01
• Series: Journal of Hainan Medical University
• Subjects: Leukemia; Atorvastatin; Apoptosis; Phosphatidylinostitol 3-kinase; Serine threonine protein kinase; Mammalian target of rapamycin
• Online Access: http://www.jhmuweb.net/PDF/201606/3.pdf
• ISSN: 1007-1237; 1007-1237

Objective: To study the regulatory effect of atorvastatin on HL-60 leukemia cell apoptosis through PI3K/AKT/mTOR. Methods: HL-60 leukemia cells were cultured and processed with different doses of atorvastatin, and then cell apoptosis as well as PI3K, AKT and mTOR expression levels were detected; cells were processed with PI3K, AKT and mTOR inhibitors Wortmannin, Perifosine and Rapamycin, and then cell apoptosis was detected. Results: Different doses of atorvastatin processing could increase the numbers of early apoptotic cells and apoptotic-like necrotic cells, and decrease mRNA contents of PI3K, AKT and mTOR in dose-dependent and time-dependent manner; PI3K, AKT and mTOR inhibitors Wortmannin, Perifosine and Rapamycin processing could increase the numbers of early apoptotic cells and apoptotic-like necrotic cells, and up-regulate the expression of apoptosis genes FasL, Bax, Caspase-3 and Caspase-9. Conclusion: Atorvastatin can induce HL-60 leukemia cell apoptosis through inhibiting PI3K/AKT/mTOR signaling pathway.