NOL8, the binding protein for beta-catenin, promoted the growth and migration of prostate cancer cells

Overactivation of beta-catenin/TCF signaling in prostate cancer is very common. However, how the beta-catenin/TCF complex is regulated in the nucleus remains largely unknown. In this study, we have shown that NOL8, a binding protein of beta-catenin, enhanced the interaction between beta-catenin and...

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Bibliographic Details
Published in:Chemico-biological interactions 2018-10, Vol.294, p.40-47
Main Authors: Gu, Shuo, Hou, Peijin, Liu, Kun, Niu, Xiaobing, Wei, Bingjian, Mao, Fei, Xu, Zongyuan
Format: Article
Language:English
Subjects:
Beta-catenin/TCF signaling
Cell growth and migration
NOL8
Prostate cancer
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Summary:Overactivation of beta-catenin/TCF signaling in prostate cancer is very common. However, how the beta-catenin/TCF complex is regulated in the nucleus remains largely unknown. In this study, we have shown that NOL8, a binding protein of beta-catenin, enhanced the interaction between beta-catenin and TCF4, and activated beta-catenin/TCF signaling. NOL8 is up-regulated in the prostate cancer, and promoted the growth, migration and colony formation of cancer cells. Knocking down the expression of NOL8 inhibited the growth, migration and colony formation of prostate cancer cells. The molecular mechanism study demonstrated that NOL8 promoted the migration and colony formation of cancer cells by activating beta-catenin/TCF signaling. Taken together, this study demonstrated the oncogenic roles of NOL8 in prostate cancer and suggested that NOL8 might be an important therapeutic target for prostate cancer. •NOL8 was up-regulated in the prostate cancer.•NOL8 activated beta-catenin/TCF signaling.•NOL8 enhanced the interaction between beta-catenin and TCF4.
ISSN:0009-2797
1872-7786
DOI:10.1016/j.cbi.2018.08.019