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MiR‐137 inhibits cell proliferation in acute lymphoblastic leukemia by targeting JARID1B
Author(s) -
Huang Yiqun,
Zou Yong,
Zheng Ruiji,
Ma Xudong
Publication year - 2019
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/ejh.13276
Subject(s) - cell growth , gene silencing , cell culture , cell , microbiology and biotechnology , apoptosis , h3k4me3 , cancer research , chemistry , biology , gene expression , gene , promoter , genetics , biochemistry
Aim 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 JARID1B and 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.