Overexpressed miR-122-5p Promotes Cell Viability, Proliferation, Migration And Glycolysis Of Renal Cancer By Negatively Regulating PKM2.
Cancer Manag Res
; 11: 9701-9713, 2019.
Article
em En
| MEDLINE
| ID: mdl-31814765
ABSTRACT
OBJECTIVE:
Renal cancer is one of the most deadly urological malignancies. Currently, there is still a lack of effective treatment. Our purpose was to explore the mechanisms of miR-122-5p in renal cancer.METHODS:
The expression levels of miR-122-5p and pyruvate kinase M2 (PKM2) in renal cancer cells were detected by RT-qPCR and Western blot analyses, respectively. Then, we measured the cell viability after knockdown of miR-122-5p and PKM2 using CCK-8 assay. Moreover, flow cytometry was used to investigate cell cycle and apoptosis of renal cancer cells. The cell migration of renal cancer cells transfected by miR-122-5p inhibitor and siPKM2 was then detected by wound healing assay. Furthermore, glucose consumption and lactate production were measured. Autophagy-related protein LCII/I was detected by Western blot.RESULTS:
MiR-122-5p was upregulated in renal cancer cells compared to HK2 cells, especially in 786-O cells. We found that silencing miR-122-5p promoted PKM2 expression in 786-O cells. After transfection of siPKM2 or miR-122-5p inhibitor, the cell viability of 786-O cells was significantly reduced. Furthermore, the G1 phase of 786-O cells was significantly blocked, and the S phase was significantly increased. In addition, knockdown of miR-122-5p or PKM2 promoted renal cancer cell apoptosis and inhibited cell migration. Glucose consumption of 786-O cells was significantly increased after transfection by siPKM2. Silencing miR-122-5p significantly promoted the expression levels of LCII/I.CONCLUSION:
Our findings revealed that overexpressed miR-122-5p promotes renal cancer cell viability, proliferation, migration, glycolysis and autophagy by negatively regulating PKM2, which provide a new insight for the development of renal cancer therapy.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Cancer Manag Res
Ano de publicação:
2019
Tipo de documento:
Article