Mechanism of microRNA-106a promoting invasion of breast cancer MDA-MB-231 cells / 中国病理生理杂志
Chinese Journal of Pathophysiology
;
(12): 1031-1036, 2018.
Article
in Chinese
| WPRIM
| ID: wpr-701235
ABSTRACT
AIM:
To investigate the possible mechanism of microRNA-106a promoting the invasion of human breast cancer MDA-MB-231 cells.METHODS:
The efficiencies of transfection with microRNA-106a inhibitor and mi-croRNA-106a mimic by liposome were detected by qPCR. The mRNA and protein expression levels of tissue inhibitor of metalloproteinase 2 (TIMP-2), matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) in the MDA-MB-231 cells transfected with microRNA-106a mimic were detected by qPCR and Western blot. The effect of microRNA-106a on the invasion ability of MDA-MB-231 cells was measured by Transwell assay. The luciferase reporter assay was used to detect the regulatory effect of microRNA-106a on the TIMP-2 pathway.RESULTS:
In the MDA-MB-231 cells, the ex-pression level of microRNA-106a decreased at 48 h after transfection with microRNA-106a inhibitor (P<0.05), and the expression level of microRNA-106a increased at 48 h after transfection with microRNA-106a mimic (P<0.05). The mi-croRNA-106a inhibitor decreased the invasion ability of MDA-MB-231 cells in vitro (P<0.05). The microRNA-106a mim-ic down-regulated the expression of TIMP-2 and up-regulated the expression of MMP2 and MMP9 (P<0.05) in the MDA-MB-231 cells. The microRNA-106a inhibitor enhanced the luciferase activity of the reporter plasmids containing the 3'-un-translated region of TIMP-2 gene (P<0.05), while the microRNA-106a mimic decreased the luciferase activity of the re-porter plasmid (P<0.05).CONCLUSION:
High expression of microRNA-106a promotes the invasion ability of breast cancer MDA-MB-231 cells in vitro, which may be related to the inhibition of TIMP-2 pathway. MicroRNA-106a plays an important role in the invasion of breast cancer MDA-MB-231 cells.
Full text:
Available
Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Chinese Journal of Pathophysiology
Year:
2018
Type:
Article
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