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Development of allosteric inhibitors of protein kinase CK2 with additional inhibitory effect on protein-protein interactions

Applicant Dr. Matthias Engel
Subject Area Pharmacy
Term from 2020 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 442811857
 
Final Report Year 2025

Final Report Abstract

The protein kinase CK2 maintains malignant potential in many types of tumors by promoting cell division, tumor-specific metabolism, protection against cell death and resistance to chemotherapeutic agents via many different signaling pathways. As a result, CK2 levels are abnormally elevated in many cancers, and a reduction in activity or protein levels has a strong antitumor effect. The conventional inhibitors of CK2, which compete with the cofactor ATP for the same highly conserved binding pocket, are often not selective, such as CX-4945, or are ineffective in inducing tumor cell death. In our project, we optimized Arylacylsulfonamide compounds with good efficacy against tumor cells and discovered a novel mechanism of action: binding to the catalytic subunit CK2α and the highly homologous isoform CK2α' induces an aggregation-prone conformational state of the proteins in the cells, which eventually leads to degradation by the proteasome (DC50 in U937 lymphoma cells = 0.33 µM). This mechanism is completely novel with CK2 and might lead to new drugs that specifically reduce the amount of CK2 protein in malignant tumor cells with strong CK2 overexpression, causing the cells to either die immediately or become more vulnerable to traditional chemotherapeutics.

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