Overexpression of OXCT1 inhibited colon cancer metastasis by regulating the CDK8-β-catenin axis (IMAGE)
Caption
(A) qPCR study on the effect of OXCT1 on β-catenin transcription levels.
(B) CPTAC database prediction of OXCT1's regulation on β-catenin protein levels.
(C) Effects of OXCT1 on the WNT pathway in HCT116.
(D) Regulation of β-catenin expression in the nucleus by OXCT1.
(E–F) Verification of OXCT1's effect on β-catenin transcriptional activity using the TOP/FOPflash dual - luciferase assay in HCT116.
(G–H) Inhibition of CDK8 restored the promotion of β-catenin by OXCT1-KO group.
(I) The CDK8 inhibitor reversed the enhanced cell migration caused by OXCT1 knockout.
(J–K) The overexpression of CDK8 rescued the inhibitory effect of β - catenin in the AdOXCT1 group.
(L) The overexpression of CDK8 rescued the inhibitory effect of AdOXCT1 on the migration of HCT116 cells.
(M) Investigation of OXCT1's effect on the interaction between CDK8 and β-catenin using IP assay in HCT116.
(N) Western blotting analysis of β-catenin in OXCT1-KO treated with 50 μg/mL of CHX. The cells were harvested at the indicated times. The knockout of OXCT1 prolonged the half-life of β-catenin protein (∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001).
Credit
Chenhao Li, Deao Gong, Xiaoqun Shan, Kang Wu, Jiayao Yang, Rong Zhang, Ye Huang, Kai Wang, Ni Tang, Yuxi Zhu
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