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"Subsequent experiments further suggested that OTUB1 promoted CRC malignancy by enhancing protein stability of β-catenin, via inhibition of its protein degradation by UPP pathway, which indicated its crucial role in enhancement of CRC tumor cellular proliferative and chemo-resistant capabilities."
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"At the same time, a high level of N-cadherin expression blocks beta-catenin entry into the nucleus [XREF_BIBR], so the changes in beta-catenin mediated by OTUB1 were observed in the cytoplasm in our model, which might be the reason why TCF1, LEF1 were not activated in our models (Additional file 11 : Figure S9)."