Abbreviations: ALL, acute lymphoblastic leukemia; AML, acute myelogenous leukemia; CML, chronic myelogenous leukemia; DMSO, dimethyl sulfoxide; H3K4, histone H3 lysine 4;H3K4me2, di-methylation of histone H3 at lysine 4; H3K4me3, tri-methylation of histone H3 at lysine 4; miRNAs, MicroRNAs; MTT, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-Htetrazolium bromide; qRT-PCR, real-time polymerase chain reaction.
AbstractAim: This study aimed to investigate the possible functions of interaction between JARID1B and miR-137 in ALL.
Methods: The levels of H3K4me3 and H3K4me2 and the expression of JARID1Band miR-137 were analyzed in six ALL cell lines and 30 ALL patients. The effects of miR-137 and JARID1B on cell proliferation and apoptosis were investigated by silencing or promoting the respective genes. The interaction between miR-137 and JARID1B was confirmed by double-luciferase report assay.
Results:The histone H3K4 expressions and miR-137 expression were lower in 30 ALL patients and in six ALL cell lines, while the expression of JARID1B was elevated. A negative correlation was observed between JARID1B and miR-137. Over-expression of miR-137 led to decreasing cell proliferation and increasing apoptosis in MOLT-4 and BALL-1 cells. MiR-137 inhibitor up-regulated JARID1B in these two cell lines, while promoted proliferation in BALL-1 cells only. Dual-luciferase report assay suggested that JARID1B was a direct target of miR-137 in ALL cell lines.
Conclusions:The expression of miR-137 was declined in ALL, and JARID1B was directly repressed by miR-137. Aberrant JARID1B expression could result in abnormal histone methylation, which might be one cause of ALL.
K E Y W O R D Sadult acute lymphoblastic leukemia, lymphoblastic leukemia, MiR-137