Study Overexpression Of GLIPR1 Inhibits C-myc Induced Differentiation Of Leukemic Cells

Objective: In acute myeloid leukemia(AML),up-regulated the expression level of GLIPR1,to observe the effect of C-myc,and the effect on differentiation,proliferation and apoptosis in AML cell.And explore the relationship between GLIPR1 gene and the occurrence and development of AML.Methods: The GLIPR1 expression vector and empty vector were transfected into HL-60 leukemia cell lines and Kasumi-1 cell lines by liposome,respectively.And the recombinant cell lines and the control cell lines were obtained.RT-PCR detect the expression of GLIPR1 gene,Western blot detect the protein expression level of GLIPR1 and C-myc.Cell proliferation change were detected by MTT.The CD11 expression and cell apoptosis were detected by flow cytometry cell technology.Results:(1)The mRNA and protein levels of GLIPR1 in the recombinant cell lines(pcDNA3.1-GLIPR1-HL-60 and pcDNA3.1-GLIPR1-Kasumi-1)were significantly higher than those in the empty vector control group and untransfected group(P < 0.05).(2)The expression level of C-myc protein in the recombinant cell line was significantly lower than that in the empty vector control group and untransfected group(P < 0.05),and the high expression of GLIPR1 could decrease the expression of C-myc protein in AML cells.(3)The expression level of CD11 b in the recombinant cell lines was significantly higher than that in the empty vector control group and untransfected group(P < 0.05),which indicated that the high expression of GLIPR1 could induce the differentiation of AML cells.(4)MTT detection showed that over expression of GLIPR1 in the recombinant cell lines could significantly inhibit the proliferation of AML cells(P < 0.05).(5)Flow cytometry showed that overexpression of GLIPR1 could significantly promote the apoptosis of AML cells(P < 0.05).Conclusion:(1)There were overexpression of GLIPR1 and low expression of C-myc that played important role in the development of AML.(2)The overexpression of GLIPR1 could inhibit C-myc and depress the proliferation and promote apoptosis and induce differentiation in AML cells.