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Oncotarget. 2016 Dec 27;7(52):87361-87372. doi: 10.18632/oncotarget.13571.

Targeting protein kinase CK2 suppresses bladder cancer cell survival via the glucose metabolic pathway.

Author information

1
Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

Abstract

Casein kinase 2 (CK2) is a constitutively active serine/threonine kinase that promotes cell proliferation and resists apoptosis. Elevated CK2 expression has been demonstrated in several solid tumors. The expression of CK2α in bladder cancer was elevated in tumor tissues compared with that in adjacent normal tissues. Amplified expression of CK2α was highly correlated with histological grade in bladder cancer(P = 0.024). Knockdown of CK2α in bladder cancer cell lines resulted in a reduction in tumor aerobic glycolysis, accompanied with lower phosphorylated AKT. Moreover, low CK2α levels suppressed cell growth, and similar results could be reproduced after treatment with CX-4945 with a dose-dependent response. CX-4945 inhibited migration and induced apoptosis. Furthermore, knockdown of CK2α decreased the tumorigenicity of bladder cancer cells in vivo. This study is the first to report that CK2 increases glucose metabolism in human bladder cancer. Blocking CK2 function may provide novel diagnostic and potential therapeutic.

KEYWORDS:

CK2α; bladder cancer; glycolysis; oncogene; prognosis

PMID:
27888634
PMCID:
PMC5349994
DOI:
10.18632/oncotarget.13571
[Indexed for MEDLINE]
Free PMC Article

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