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Anti-Cancer Potential of a new Derivative of Caffeic Acid Phenethyl Ester targeting the Centrosome

C. Giordano, J. Kendler, M. Sexl, S. Kollman, M. Varenicja, B. Szabó, G. Timelthaler, D. Kirchhofer, O. Hollóczki, SD. Turner, R. Moriggl, L. Kenner, M. Touaibia, O. Merkel

. 2025 ; 81 (-) : 103582. [pub] 20250305

Language English Country Netherlands

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc25009317

Anaplastic Large Cell Lymphoma (ALCL) is an aggressive T-cell lymphoma affecting children and young adults. About 30% of patients develop therapy resistance therefore new precision medicine drugs are highly warranted. Multiple rounds of structure-activity optimization of Caffeic Acid Phenethyl Ester have resulted in CM14. CM14 causes upregulation of genes involved in oxidative stress response and downregulation of DNA replication genes leading to G2/M arrest and subsequent apoptosis induction. In accordance with this, an unbiased proteomics approach, confocal microscopy and molecular modeling showed that TUBGCP2, member of the centrosomal γ-TuRC complex, is a direct interaction partner of CM14. CM14 overcomes ALK inhibitor resistance in ALCL and is also active in T-cell Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia. Interestingly, CM14 also induced cell death in docetaxel-resistant prostate cancer cells thus suggesting an unexpected role in solid cancers. Thus, we synthesized and thoroughly characterized a novel TUBGCP2 targeting drug that is active in ALCL but has also potential for other malignancies.

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$a Anaplastic Large Cell Lymphoma (ALCL) is an aggressive T-cell lymphoma affecting children and young adults. About 30% of patients develop therapy resistance therefore new precision medicine drugs are highly warranted. Multiple rounds of structure-activity optimization of Caffeic Acid Phenethyl Ester have resulted in CM14. CM14 causes upregulation of genes involved in oxidative stress response and downregulation of DNA replication genes leading to G2/M arrest and subsequent apoptosis induction. In accordance with this, an unbiased proteomics approach, confocal microscopy and molecular modeling showed that TUBGCP2, member of the centrosomal γ-TuRC complex, is a direct interaction partner of CM14. CM14 overcomes ALK inhibitor resistance in ALCL and is also active in T-cell Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia. Interestingly, CM14 also induced cell death in docetaxel-resistant prostate cancer cells thus suggesting an unexpected role in solid cancers. Thus, we synthesized and thoroughly characterized a novel TUBGCP2 targeting drug that is active in ALCL but has also potential for other malignancies.
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$a Kendler, Jonatan $u Department of Biological Sciences and Pathobiology, Pharmacology and Toxicology, University of Veterinary Medicine Vienna, Vienna, Austria
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$a Sexl, Maximilian $u Department of Biological Sciences and Pathobiology, Pharmacology and Toxicology, University of Veterinary Medicine Vienna, Vienna, Austria
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$a Kollman, Sebastian $u Department of Biological Sciences and Pathobiology, Pharmacology and Toxicology, University of Veterinary Medicine Vienna, Vienna, Austria
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$a Varenicja, Maxim $u Department of Physical Chemistry, University of Debrecen, Debrecen, Hungary
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$a Szabó, Boglárka $u Department of Physical Chemistry, University of Debrecen, Debrecen, Hungary
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$a Timelthaler, Gerald $u Center for Cancer Research, Medical University of Vienna, Vienna, Austria
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$a Kirchhofer, Dominik $u Center for Cancer Research, Medical University of Vienna, Vienna, Austria
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$a Hollóczki, Oldamur $u Department of Physical Chemistry, University of Debrecen, Debrecen, Hungary
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$a Turner, Suzanne D $u European Research Initiative on ALK-Related Malignancies (ERIA), Cambridge, UK; Division of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK; Faculty of Medicine, Masaryk University, Brno, Czech Republic
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$a Moriggl, Richard $u Department of Biosciences and Medical Biology, Paris Lodron University of Salzburg, Salzburg, Austria
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$a Kenner, Lukas $u Department of Pathology, Medical University of Vienna, Vienna, Austria; European Research Initiative on ALK-Related Malignancies (ERIA), Cambridge, UK; Christian Doppler Laboratory (CDL) for Applied Metabolomics, Medical University of Vienna, Vienna, Austria; Unit of Laboratory Animal Pathology, University of Veterinary Medicine, Vienna, Austria; Center for Biomarker Research in Medicine (CBMed) Core Lab 2, Medical University of Vienna, Vienna, Austria; Department of Molecular Biology, Umeå University, Umeå, Sweden
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$a Touaibia, Mohamed $u Chemistry and Biochemistry Department, Université de Moncton, Moncton, New Brunswick, Canada. Electronic address: mohamed.touaibia@umoncton.ca
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$a Merkel, Olaf $u Department of Pathology, Medical University of Vienna, Vienna, Austria; European Research Initiative on ALK-Related Malignancies (ERIA), Cambridge, UK. Electronic address: olaf.merkel@meduniwien.ac.at
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