Oncotarget

Research Papers:

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

Xiaolei Zhang _, Xiao Yang, Chengdi Yang, Peng Li, Wenbo Yuan, Xiaheng Deng, Yidong Cheng, Pengchao Li, Haiwei Yang, Jun Tao and Qiang Lu

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:87361-87372. https://doi.org/10.18632/oncotarget.13571

Metrics: PDF 1567 views  |   HTML 2066 views  |   ?  


Abstract

Xiaolei Zhang1,*, Xiao Yang1,*, Chengdi Yang1,*, Peng Li1, Wenbo Yuan1, Xiaheng Deng1, Yidong Cheng1, Pengchao Li1, Haiwei Yang1, Jun Tao1, Qiang Lu1

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

*These authors have contributed equally to this work

Correspondence to:

Jun Tao, email: [email protected]

Qiang Lu, email: [email protected]

Keywords: bladder cancer, CK2α, glycolysis, oncogene, prognosis

Received: May 14, 2016   Accepted: November 7, 2016    Published: November 24, 2016

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.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 13571