KYA1797K down-regulates PD-L1 in colon cancer stem cells to block immune evasion by suppressing the β-catenin/STT3 signaling pathway.

KYA1797K down-regulates PD-L1 in colon cancer stem cells to block immune evasion by suppressing the β-catenin/STT3 signaling pathway. Int Immunopharmacol. 2019 Dec 04;78:106003 Authors: Ruan Z, Liang M, Lai M, Shang L, Deng X, Su X Abstract Cancer stem cells (CSCs) are considered to mediate tumorigenesis, recurrence, and metastasis. KYA1797K, a β-catenin inhibitor, has been identified for its functionality as a tumor suppressor gene in colorectal cancer through inhibition of the Wnt/β-catenin signaling pathway. However, it remains uncertain whether KYA1797K attenuates immune evasion of colon CSCs. Hence, this study is designed for evaluating the function of KYA1797K in colon CSCs. The expression of β-catenin and STT3A/B in colon cancer tissues was initially detected by immunohistochemistry, followed by correlation analyses of the survival rate with the expression of β-catenin and STT3A/B as well as identification of the interaction between β-catenin and STT3A/B. Besides, β-catenin in colon CSCs was knocked down or inhibited by KYA1797K to explore its role in immune evasion and the subsequent underlying mechanism associated with STT3A/B expression and PD-L1 glycosylation. Additionally, the in vivo regulatory effects of β-catenin silencing and KYA1797K were evaluated by assessing tumor formation, detecting CD8 and GZMB expression and CD8+ T cell viability. The results collected displayed that β-catenin and STT3A/B showed high ...
Source: International Immunopharmacology - Category: Allergy & Immunology Authors: Tags: Int Immunopharmacol Source Type: research