Abstract:
: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.
journal_name
Chem Biol Interactjournal_title
Chemico-biological interactionsauthors
Gu S,Hou P,Liu K,Niu X,Wei B,Mao F,Xu Zdoi
10.1016/j.cbi.2018.08.019subject
Has Abstractpub_date
2018-10-01 00:00:00pages
40-47eissn
0009-2797issn
1872-7786pii
S0009-2797(18)30169-8journal_volume
294pub_type
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journal_title:Chemico-biological interactions
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journal_title:Chemico-biological interactions
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