Objective To investigate the effect of quercetin on PML gene and protein expression andlocalization in leukemia cell lines. Methods Cell morphology was assayed by Wright's stain and fluorescence stain, and PML mRNA expression by RT-PCR , PML protein localization by immuno-fluorescence. Results NB4 and HL-60 cells differentiated morphologically after treatment with all-trans-retinoic acid (ATRA) while K562 cells did not differentiate. Typical apoptosis was found in each cell line after treatment with quercetin. Immuno-fluorescence analysis showed , after treatment with ATRA , the fusion protein disappeared in NB4 cells and PML protein relocated , while HL-60 and K562 cells had no difference from control cells. After treatment with quercetin, the fusion protein disappeared in NB4 cells, PML protein relocated, then degraded. In HL-60 cells and K562 cells, PML protein also located and then degraded . The expression of PML mRNA was not changed in all three cell lines after treatment with ATRA or quercetin. Conclusion PML plays the role of differentiation and apoptosis inducer in leukemia cells at the translational level. PML in POD plays the role of apoptosis inducer and the growth control of leukemia cells.
Objective To investigate the effects of quercetin on cell morphology, expression of promye-locytic leukemia (PML) mRNA and PML protein localization of NB4, HL-60 cells. Methods Cells mor-phology assayed by Wright’ s stain, fluorescence stain, and PML mRNA expression by RT-PCR, PML protein localization by immuno-fluorescence. Results The typical apoptosis was found in NB4 and HL-60 cells after treatment with quercetin. Immuno-fluorescence analysis showed after treatment with quercetin, the fusion pro-tein disappeared in NB4 cells, PML protein relocated, then degraded, and that also seen in HL-60 cells. The expression of PML mRNA is not changed in quercetin-treated cells. Conclusion PML play the role of apop-tosis inducer in leukemia cells at the translational level, quercetin can inhibit the proliferation of leukemia cells, and induce NB4, HL-60 cells apoptosis.
Objective :To investigate PML. gene and protein expression and localization in leukemia cell lines. Methods Cell morphology was assayed by Wright’s stain and fluorescence stain, and PML mRNA expression by RT-PCR, PML protein localization by immuno-fluorescence. Results NB4 and HL-60 cells differentiated morphologically after treatment with anti-retinoic acid (ATRA ) while K562 cells did not differentiate. Typical apoptosis was found in each cell line after treatment with red orpiment. Immuno-fluorescence analysis showed, after treatment with ATRA, the fusion protein disappeared in NB4 cells and the PML protein relocated, while HL-60 and K562 cells had no difference from control cells. After treatment with red orpiment, the fusion protein disappeared in NB4 cells, then degraded, which was also seen in HL-60 cells and K562 cells. The expression of PML mRNA was not changed in all three cell lines after treatment with ATRA or red orpiment. Conclusion PML plays the role of differentiation and apoptosis inducer in leukemia cells at the translational level. PML in POD plays the role of apoptosis inducer and the growth control of leukemia cells.
