[Autophagy and Expression of UCH-L3 Induced by Rapamycin in HL-60 Cells]

The aim of this study was to explore whether rapamycin can induce the autophagy of HL-60 cells and UCH-L3 expression.

Cell proliferation activity of HL-60 cells treated with rapamycin was measured by CCK-8 assay. After the cells were treated with rapamycin for different time, the fluorescent microscopy was used to detect the cells' modality, the morphology of autophagosomes was observed by transmission electron microscopy, the mRNA levels of autophagy-related genes LC3-II and UCH-L3 were detected by real-time PCR, and the Western blot was employed to detect the expression level of UCH-L3.

Different concentrations of rapamycin could inhibit the proliferation of HL-60 cells. The inhititory levels in treatment groupall were statistically different from those in the control group (P<0.05). Under fluorescent microscopy, the fluorescence intensity in the control group was low, but in the treatment groups it strengthened along with the extension of process time. After treatmant with 2µmol/L rapamycin for different time (12、24 h), the number of autophagosomes in the control group was less , while in the treatment groups was more, the mRNA level of LC3-II was raised as compared with the control group, while the mRNA and protein level of UCH-L3 declined (P<0.05).

Rapamycin can inhibit the proliferation of HL-60 cells and induce the autophagic death. UCH-L3 may play a role in the regulation of autophagic death of leukemia.