MCC1019, a selective inhibitor of the Polo-box domain of Polo-like kinase 1 as novel, potent anticancer candidate.

3-MA, 3-methyladenine ABC, avidin-biotin complex APC/C, anaphase-promoting complex/cyclosome BUBR1, budding uninhibited by benzimidazole-related 1 CDC2, cell division cycle protein 2 homolog CDC25, cell division cycle 25 CDK, cyclin-dependent kinase Cell cycle DAPI, 4′,6-diamidino-2-phenylindole DAPKs, death-associated protein kinase FBS, fetal bovine serum FOXO, forkhead box O HIF-1α, hypoxia-inducible factor 1 α IC50, 50% inhibition concentration IHC, immunohistochemistry Kd, the dissociation constant LC3, light chain 3 MFP, M phase promoting factor MST, microscale thermophoresis MTD, maximal tolerance dose Mono-targeted therapy Nec-1, necrostatin 1 Necroptosis PARP-1, poly(ADP-ribose) polymerase-1 PBD, Polo box domain PDB, Protein Data Bank PI, propidium iodide PLK1 PLK1, Polo-like kinase Polo box domain Polo-like kinase SAC, spindle assembly checkpoint Spindle damage

Journal

Acta pharmaceutica Sinica. B
ISSN: 2211-3835
Titre abrégé: Acta Pharm Sin B
Pays: Netherlands
ID NLM: 101600560

Informations de publication

Date de publication:
Sep 2019
Historique:
received: 23 08 2018
revised: 20 12 2018
accepted: 22 12 2018
entrez: 26 10 2019
pubmed: 28 10 2019
medline: 28 10 2019
Statut: ppublish

Résumé

Polo-like kinase (PLK1) has been identified as a potential target for cancer treatment. Although a number of small molecules have been investigated as PLK1 inhibitors, many of which showed limited selectivity. PLK1 harbors a regulatory domain, the Polo box domain (PBD), which has a key regulatory function for kinase activity and substrate recognition. We report on 3-bromomethyl-benzofuran-2-carboxylic acid ethyl ester (designated: MCC1019) as selective PLK1 inhibitor targeting PLK1 PBD. Cytotoxicity and fluorescence polarization-based screening were applied to a library of 1162 drug-like compounds to identify potential inhibitors of PLK1 PBD. The activity of compound MC1019 against the PLK1 PBD was confirmed using fluorescence polarization and microscale thermophoresis. This compound exerted specificity towards PLK1 over PLK2 and PLK3. MCC1019 showed cytotoxic activity in a panel of different cancer cell lines. Mechanistic investigations in A549 lung adenocarcinoma cells revealed that MCC1019 induced cell growth inhibition through inactivation of AKT signaling pathway, it also induced prolonged mitotic arrest-a phenomenon known as mitotic catastrophe, which is followed by immediate cell death

Identifiants

pubmed: 31649851
doi: 10.1016/j.apsb.2019.02.001
pii: S2211-3835(18)30827-X
pmc: PMC6804483
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1021-1034

Informations de copyright

© 2019 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.

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Auteurs

Sara Abdelfatah (S)

Department of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, Johannes Gutenberg University, Mainz 55128, Germany.

Angela Berg (A)

Leipzig University, Institute of Organic Chemistry, Leipzig 04103, Germany.

Qi Huang (Q)

State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.

Li Jun Yang (LJ)

State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.

Sami Hamdoun (S)

Department of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, Johannes Gutenberg University, Mainz 55128, Germany.

Anette Klinger (A)

MicroCombiChem GmbH, Wiesbaden 65203, Germany.

Henry J Greten (HJ)

Abel Salazar Institute of Biomedical Sciences, University of Porto, Porto 4099-003, Portugal.

Edmond Fleischer (E)

MicroCombiChem GmbH, Wiesbaden 65203, Germany.

Thorsten Berg (T)

Leipzig University, Institute of Organic Chemistry, Leipzig 04103, Germany.

Vincent K W Wong (VKW)

State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.

Thomas Efferth (T)

Department of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, Johannes Gutenberg University, Mainz 55128, Germany.

Classifications MeSH