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. 2022 Apr 12;12:844477. doi: 10.3389/fonc.2022.844477

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Copyright © 2022 Ning, Sun, Su, Tan, Tang, Sayed, Li, Xue, Liu, Chen and Lu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Depletion of CK1δ/ϵ or treatment with CK1 inhibitors downregulate the level of β-catenin acetylation at K49 in colon cancer cells. (A, B) The expression of endogenous CK1δ and CK1ϵ was knocked down by infecting SW480 (A) and HCT116 (B) cells with shNC, shCK1δ-1, shCK1δ-2, shCK1ϵ-1, shCK1ϵ-2 and shCK1δ/ϵ-2 lentivirus. The levels of β-catenin, acetylated β-catenin at K49, CK1δ, CK1ϵ and GAPDH were detected by immunoblotting. (C, D) SW480 (C) and HCT116 (D) cells were serum-starved for 12 h and subsequently treated with the indicated amounts of SR3029 for 12 h Cell lysates were subjected to immunoblotting with the indicated antibodies. (E, F) Similar to panel C and D except that the indicated concentrations of D4476 were used. (G, H) Similar to panel (C, D) except that the indicated concentrations of longdaysin were used.