Title : The anthelmintic drug niclosamide induces GSK-β-mediated β-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability and suppress pancreatic cancer progression.

Pub. Date : 2022 Feb 3

PMID : 35115509






7 Functional Relationships(s)
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1 The anthelmintic drug niclosamide induces GSK-beta-mediated beta-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability and suppress pancreatic cancer progression. Niclosamide catenin (cadherin associated protein), beta 1 Mus musculus
2 Mechanistically, niclosamide exerted these therapeutic effects via targeting beta-catenin. Niclosamide catenin (cadherin associated protein), beta 1 Mus musculus
3 Moreover, niclosamide induced beta-catenin phosphorylation and protein degradation. Niclosamide catenin (cadherin associated protein), beta 1 Mus musculus
4 Interestingly, niclosamide also induced GSK-3beta phosphorylation, which is involved in the ubiquitination degradation of beta-catenin. Niclosamide catenin (cadherin associated protein), beta 1 Mus musculus
5 Pharmacological activation of beta-catenin by methyl vanillate and beta-catenin overexpression abolished the inhibitory effects of niclosamide. Niclosamide catenin (cadherin associated protein), beta 1 Mus musculus
6 Pharmacological activation of beta-catenin by methyl vanillate and beta-catenin overexpression abolished the inhibitory effects of niclosamide. Niclosamide catenin (cadherin associated protein), beta 1 Mus musculus
7 Thus, our study indicated that niclosamide induces GSK-beta-mediated beta-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability, and suppress pancreatic cancer progression. Niclosamide catenin (cadherin associated protein), beta 1 Mus musculus