ABSTRACT
OBJECTIVE@#To study the expression of microRNA-130b (miR-130b) in children acute promyelocytic leukemia (APL) and its role for regulating PTEN expression.@*METHODS@#A total of 50 children APL marrow tissues and 15 normal marrow tissues between January and December in 2012 were collected into our study. The expression of miR-130b in APL and normal marrow tissues were detected by quantitative real-time polymerase chain reaction. MiR-130b inhibitor was transfected into HL-60 cells. Cell Counting Kit-8 assay and flow cytometry were used to measure cell proliferation and apoptosis, respectively. The expression of PTEN, a potential target of miR-130b, and its downstream genes, Bcl-2 and Bax, in transformed cells were detected by quantitative real-time polymerase chain reaction and western-blot.@*RESULTS@#The expression of miR-130b was significantly higher in children APL marrow tissues than in normal marrow tissues (P < 0.05). Down-regulation of miR-130b could significantly suppress cell proliferation and induce apoptosis in HL-60 cells (P < 0.05). PTEN expression was upregulated when miR-130b was knocking-down (P < 0.05). As downstream genes of PTEN, the expression of Bcl-2 and Bax were regulated as well.@*CONCLUSIONS@#MiR-130b is overexpressed in children APL marrow tissues and associated with cell growth. MiR-130b may promote children APL progression by inducing cell proliferation and inhibiting apoptosis.
ABSTRACT
Objective: To study the expression of microRNA-130b (miR-130b) in children acute promyelocytic leukemia (APL) and its role for regulating PTEN expression. Methods: A total of 50 children APL marrow tissues and 15 normal marrow tissues between January and December in 2012 were collected into our study. The expression of miR-130b in APL and normal marrow tissues were detected by quantitative real-time polymerase chain reaction. MiR-130b inhibitor was transfected into HL-60 cells. Cell Counting Kit-8 assay and flow cytometry were used to measure cell proliferation and apoptosis, respectively. The expression of PTEN, a potential target of miR-130b, and its downstream genes, Bcl-2 and Bax, in transformed cells were detected by quantitative real-time polymerase chain reaction and western-blot. Results: The expression of miR-130b was significantly higher in children APL marrow tissues than in normal marrow tissues (P < 0.05). Down-regulation of miR-130b could significantly suppress cell proliferation and induce apoptosis in HL-60 cells (P < 0.05). PTEN expression was upregulated when miR-130b was knocking-down (P < 0.05). As downstream genes of PTEN, the expression of Bcl-2 and Bax were regulated as well. Conclusions: MiR-130b is overexpressed in children APL marrow tissues and associated with cell growth. MiR-130b may promote children APL progression by inducing cell proliferation and inhibiting apoptosis.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate whether P-selectin gene -2123 polymorphism is associated with the pathogenesis of Henoch-Sch-nlein purpura (HSP) in children.</p><p><b>METHODS</b>Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) is used to identify the distribution of allele and genotype frequencies of P-selectin gene promoter -2123 polymorphism in 86 children with HSP (including 40 cases of purpura nephritis) and 70 healthy controls.</p><p><b>RESULTS</b>Compared with the healthy controls, the frequencies of GG genotype and G allele of P-selectin promoter -2123 in children with HSP increased significantly (P<0.05). There were no significant differences in P-selectin promoter -2123 genotype and allele frequencies between the patients with and without nephritis.</p><p><b>CONCLUSIONS</b>P-selectin gene promoter -2123 polymorphism appears to be associated with the pathogenesis of HSP in children.</p>