- Author:
Huan WANG
1
;
Jing LI
1
;
Yan-Chun LIU
2
;
Xi CHEN
1
;
Tie CHAI
1
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Cell Line, Tumor; Cell Proliferation; Forkhead Box Protein M1; Humans; Mice; MicroRNAs; Multiple Myeloma
- From: Journal of Experimental Hematology 2018;26(3):829-835
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the mechanism and clinical value of miR-373 in multiple myeloma.
METHODSThe expressions of miR-373 in multiple myeloma cells and normal plasma cells were detected by RT-PCR, and the biological function of miR-373 in tumor was analyzed by MTT assay, flow cytometry, luciferase experiment and tumorgenesis experiment.
RESULTSThe miR-373 expression levels in MM patients and multiple myeloma cell lines (H929, MM1S and U266) were significantly lower than that in normal plasma cells detected by using RT-PCR (P<0.05). The proliferations of U266 and H929 cells transfected with miR-373 were significantly suppressed (P<0.05); the cell cycle of H929 cell transfected with miR-373 was arrested in the G/G phase(P<0.05) and the cell apoptosis was induced (P<0.05). Luciferase experiment revealed that miR-373 could significantly inhibit the expression of FOXM1 (P<0.05). In mouse tumorigenesis experiments, overexpression of miR-373 significantly inhibited tumor growth by decreasing FOXM1 levels (P<0.05).
CONCLUSIONmiR-373 inhibits tumor growth in MM by direct targeting FOXM1, thus miR-373 shows an important clinical significance for the treatment of MM.