MiR-182-5p Knockdown Targeting PTEN Inhibits Cell Proliferation and Invasion of Breast Cancer Cells
Yonsei Medical Journal
;
: 148-157, 2019.
Article
in English
| WPRIM
| ID: wpr-742524
ABSTRACT
PURPOSE:
Breast cancer (BC) is one of the most common malignant tumors, affecting a significant number of women worldwide. MicroRNAs (miRNAs) have been reported to play important roles in tumorigenesis. The aim of this study was to determine the roles of miR-182-5p in BC progression. MATERIALS ANDMETHODS:
The expressions of miR-182-5p and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) were measured in BC tissues and cells by quantitative real-time polymerase chain reaction or Western blot. Cell proliferation and invasion were detected by cell counting kit-8 assay and trans-well assay, respectively. The interaction between miR-182-5p and PTEN was probed by bioinformatics analysis, luciferase activity, and RNA immunoprecipitation. A murine xenograft model was established to investigate the role of miR-182-5p in BC progression in vivo.RESULTS:
An abundance of miR-182-5p was noted in BC tissues and cells. High expression of miR-182-5p was associated with poor survival. Abrogation of miR-182-5p inhibited cell proliferation and invasion in BC cells. Interestingly, PTEN was indicated as a target of miR-182-5p, and its restoration reversed miR-182-5p-mediated promotion of proliferation and invasion of BC cells. Moreover, depletion of miR-182-5p suppressed tumor growth via up-regulating PTEN expression in the murine xenograft model.CONCLUSION:
MiR-182-5p exhaustion blocked cell proliferation and invasion by regulating PTEN expression, providing a novel therapeutic avenue for treatment of BC.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Chromosomes, Human, Pair 10
/
Breast
/
Breast Neoplasms
/
RNA
/
Cell Count
/
Blotting, Western
/
Computational Biology
/
MicroRNAs
/
Immunoprecipitation
/
Cell Proliferation
Limits:
Female
/
Humans
Language:
English
Journal:
Yonsei Medical Journal
Year:
2019
Type:
Article
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