Protein kinase CK2 activation is required for transforming growth factor β-induced epithelial-mesenchymal transition

Molecular Oncology
Seongrak KimKunhong Kim

Abstract

Transforming growth factor β (TGFβ) is overexpressed in advanced cancers and promotes tumorigenesis by inducing epithelial-mesenchymal transition (EMT), which enhances invasiveness and metastasis. Although we previously reported that EMT could be induced by increasing CK2 activity alone, it is not known whether CK2 also plays an essential role in TGFβ-induced EMT. Therefore, in the present study, we investigated whether TGFβ signaling could activate CK2 and, if so, whether such activation is required for TGFβ-induced EMT. We found that CK2 is activated by TGFβ treatment, and that activity peaks at 48 h after treatment. CK2 activation is dependent on TGFβ receptor (TGFBR) I kinase activity, but independent of SMAD4. Inhibition of CK2 activation through the use of either a CK2 inhibitor or shRNA against CSNK2A1 inhibited TGFβ-induced EMT. TGFβ signaling decreased CK2β but did not affect CK2α protein levels, resulting in a quantitative imbalance between the catalytic α and regulatory β subunits, thereby increasing CK2 activity. The decrease in CK2β expression was dependent on TGFBRI kinase activity and the ubiquitin-proteasome pathway. The E3 ubiquitin ligases responsible for TGFβ-induced CK2β degradation were found to be CHIP and...Continue Reading

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Citations

Dec 15, 2020·Frontiers in Endocrinology·Ger J StrousJan A Mol
Apr 20, 2020·Medical Hypotheses·Mark F McCartyLidianys Lewis Lujan
Jul 4, 2020·Molecular and Cellular Probes·Shuo ChenXipeng Zhang
Apr 13, 2021·Critical Reviews in Biochemistry and Molecular Biology·Christian BorgoMauro Salvi
Jul 27, 2021·Experimental and Therapeutic Medicine·Ping WangBai-Qing Wang
Jul 7, 2021·Cell Death Discovery·Xiaoli HuGang Chen

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Methods Mentioned

BETA
immunoprecipitation
gene knockout
ubiquitination

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