miR-593 inhibits proliferation of colon cancer cells by down-regulating PLK1 / 南方医科大学学报
Journal of Southern Medical University
;
(12): 144-149, 2019.
Article
in Chinese
| WPRIM
| ID: wpr-772107
ABSTRACT
OBJECTIVE@#To explore the role of miR-593 in regulating the proliferation of colon cancer cells and the molecular mechanism.@*METHODS@#Bioinformatics analysis identified PLK1 as the possible target gene of miR-593. Luciferase assay was employed to verify the binding between miR-593 and PLK1, and qRT-PCR and Western blotting were used to verify that PLK1 was the direct target gene of miR-593. CCK-8 assay was performed to test the hypothesis that miR-593 inhibited the proliferation of colon cancer cells by targeting PLK1.@*RESULTS@#Luciferase assay identified the specific site of miR-593 binding with PLK1. Western blotting showed a significantly decreased expression of PLK1 in the colon cancer cells transfected with miR-593 mimics and an increased PLK1 expression in the cells transfected with the miR-593 inhibitor as compared with the control cells ( < 0.05). The results of qRT-PCR showed no significant differences in the expression levels of PLK1 among the cells with different treatments ( > 0.05). The cell proliferation assay showed opposite effects of miR-593 and PLK1 on the proliferation of colon cancer cells, and the effect of co-transfection with miR-593 mimic and a PLK1-overexpressing plasmid on the cell proliferation was between those in PLK1 over-expressing group and miR-593 mimic group.@*CONCLUSIONS@#miR-593 inhibits the proliferation of colon cancer cells by down-regulating PLK1 and plays the role as a tumor suppressor in colon cancer.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Sincalide
/
Binding Sites
/
In Vitro Techniques
/
Transfection
/
Down-Regulation
/
Gene Expression Regulation, Neoplastic
/
Genes, Tumor Suppressor
/
Proto-Oncogene Proteins
/
Protein Serine-Threonine Kinases
Limits:
Humans
Language:
Chinese
Journal:
Journal of Southern Medical University
Year:
2019
Type:
Article
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