Rapamycin induces human acute promyelocytic leukemia cell HL-60 autophagic apoptosis

Y.-H. Zhang, Q.-F. Lin, X.-L. Wang, Q.-Y. Li, J.-J. Chai, X.-J. Fan

Department of Gastroenterology, People’s Hospital of Weifang, Weifang, Shandong, China. 13964063337@139.com

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• Pharmacology

OBJECTIVE: We aimed at investigating the effects of rapamycin on apoptosis and autophagy of human acute promyelocytic leukemia cell line HL-60, and to preliminarily explore the mechanism of extra medullary infiltration of leukemia cells with human acute promyelocytic leukemia cell line HL-60 as the object of study, providing a theoretical basis for the clinical treatment of leukemia.

MATERIALS AND METHODS: After HL-60 cells were cultured in vitro, the effect of rapamycin on proliferation ability of HL-60 cells was determined by methyl thiazolyl tetrazolium (MTT) method, the cell apoptosis ratio was detected by flow cytometer, the change of autophagy after HL-60 cells acted by rapamycin was tested by monodansylcadaverine (MDC) fluorescence staining, the mRNA expression of autophagy-related molecule was detected by polymerase chain reaction (PCR), and the expressions of apoptosis-related protein and autophagy-related protein were determined by Western blotting (WB).

RESULTS: HL-60 cell proliferation could be significantly inhibited by rapamycin (80 μg/mL-640 μg/mL), which was in a dose-dependent manner. HL-60 cell apoptosis ratio and apoptosis-related protein expression were distinctly improved by rapamycin. Cell autophagy level, mRNA expression of autophagy-related molecule and autophagy-related protein expression were remarkably induced by rapamycin.

CONCLUSIONS: Rapamycin can induce HL-60 cell apoptosis, which is produced mainly by inducing cell autophagy.

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