The Effect Of Over-expressing JMJD3Gene By Eukaryotic Vector In Acute Leukemia Cell Line HL-60

Objective: To study the state of histone trimethylated H3K27and histonedemethylase JMJD3in acute leukemic cell lines, HL-60, U937and NB4. We furtherobserved the cell growth and apoptosis in HL-60cell line and investigatedpathogenesis of JMJD3in acute leukemic cell in vitro and possibility of JMJD3geneas target for leukemia therapy.Results:(1) The histone H3K27me3was high expression and demethylase JMJD3was low expression in three acute leukemia cell, i.e. HL-60, U937and NB4.(2) After48hours Pegfp-C3-JMJD3transfection, the efficiency reached70%±2.34%.(3) Thecell proliferation was decreased obviously in (68.54±0.73)%,(49.10±2.31)%,(41.22±1.01)%and (40.68±2.45)%respectively after Pegfp-C3-JMJD3transfectionfor48,72,96and120hrs, which was lower than that in negative control and blankcontrol (p<0.05). The proportion of cell G2/M phase was (46.02±0.92)%, which washigher than that in blank control (18.56±3.71)%and negative control (22.86±1.45)%(p<0.05). S phase was (10.94±1.78)%, which was lower than that in blank control(33.54±1.41)%, and negative plasmid control (33.24±1.05)%, p <0.05. Overexpression of JMJD3upregulated P15and P16in2.13folds and2.07foldsrespectively, and it downregulated H3K27me3in78.54%(p <0.05).Conclusions:(1) Aberrant histone demethylase JMJD3and H3K27me3is existed inacute leukemic cell HL-60, U937and NB4. JMJD3gene might be related topathogenesis in acute leukemia.(2) Over expression of JMJD3gene inhibit HL-60cell proliferation, accumulated cell cycle in G2/M phase, induced cell apoptosis. Itup-regulate the expression of P15and P16, which might be one of the mechanisms forJMJD3gene as anticancer target.