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MicroRNA‐9 suppresses cancer proliferation and cell cycle progression in acute lymphoblastic leukemia with inverse association of neuropilin‐1
Author(s) -
Zang Yuzhu,
Yu Runhong,
Bai Yanliang,
Chen Xiangli
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26799
Subject(s) - cell growth , neuropilin 1 , downregulation and upregulation , cancer research , microrna , cell cycle , biology , cell culture , cell , gene , biochemistry , genetics , vascular endothelial growth factor , vegf receptors
Abstract Acute lymphoblastic leukemia (ALL) is one of the most common and most malign childhood cancers. In this work, we investigated the expression and function of human mature microRNA‐9 (miR‐9) in ALL. In ALL in vitro cell lines and in situ clinical specimens, gene expression of miR‐9 was tested by qRT‐PCR. MiR‐9 was overexpressed in CEM/C1 and Molt‐3 cells to investigate its possible anti‐cancer effects on ALL in vitro proliferation, cell‐cycle progression, and in vivo explant growth. The possible downstream target of miR‐9, neuropilin‐1 (NRP1), was examined by dual‐luciferase activity assay, qRT‐PCR, and Western blot. NRP1was upregulated in miR‐9‐overexpressed CEM/C1 and Molt‐3 cells to investigate the functional involvement of NRP1 in miR‐9‐mediated regulation on ALL in vitro proliferation and cell‐cycle progression. MiR‐9 was downregulated in ALL cell lines and leukemic T‐cells of ALL patients. Lentivirus‐mediated miR‐9 overexpression inhibited ALL in vitro proliferation, cell‐cycle progression, and in vivo explant growth. NRP1 was confirmed be the downstream target of miR‐9, and inversely modulated by miR‐9 in ALL. NRP1 upregulation reversed the anti‐cancer regulations of miR‐9 on ALL in vitro proliferation and cell‐cycle progression. MiR‐9 is downregulated in ALL. Overexpressing miR‐9 may inhibit ALL development, possible through its downstream target of NRP1.