Overexpressed miR-122-5p Promotes Cell Viability, Proliferation, Migration And Glycolysis Of Renal Cancer By Negatively Regulating PKM2
Authors Wang S, Zheng W, Ji A, Zhang D, Zhou M
Received 2 August 2019
Accepted for publication 25 October 2019
Published 15 November 2019 Volume 2019:11 Pages 9701—9713
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Cristina Weinberg
Peer reviewer comments 2
Editor who approved publication: Dr Chien-Feng Li
Shuai Wang, Wei Zheng, Alin Ji, Dahong Zhang, Mi Zhou
Department of Urology, Zhejiang Provincial People’s Hospital, People’s Hospital of Hangzhou Medical College, Hangzhou 310014, Zhejiang Province, People’s Republic of China
Correspondence: Mi Zhou
Department Of Urology, Zhejiang Provincial People’s Hospital, People’s Hospital Of Hangzhou Medical College, No. 158 Shangtang Road, Xiacheng District, Hangzhou 310014, Zhejiang Province, People’s Republic of China
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.
Keywords: PKM2, miR-122-5p, cell viability, glycolysis, renal cancer
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