RO3280: A Novel PLK1 Inhibitor, Suppressed the Proliferation of MCF-7 Breast Cancer Cells Through the Induction of Cell Cycle Arrest at G2/M Point

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dc.authoridErgul, Mustafa/0000-0003-4303-2996
dc.authoridBAKAR ATES, FILIZ/0000-0003-2809-8946
dc.contributor.authorErgul, Mustafa
dc.contributor.authorBakar-Ates, Filiz
dc.date.accessioned2024-10-26T18:07:16Z
dc.date.available2024-10-26T18:07:16Z
dc.date.issued2019
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractBackground: As a member of serine/threonine-protein kinase, Polo-like kinase 1 (PLK1) plays crucial roles during mitosis and also contributes to DNA damage response and repair. PLK1 is aberrantly expressed in many types of tumor cells and increased levels of PLK1 are closely related to tumorigenesis and poor clinical outcomes. Therefore, PLK1 is accepted as one of the potential targets for the discovery of novel anticancer agents. The objective of this study was to assess the cytotoxic effects of a novel PLK1 inhibitor, RO3280, against MCF-7, human breast cancer cells; HepG2, human hepatocellular carcinoma cells; and PC3, human prostate cancer cells, as well as non-cancerous L929 fibroblast cells. Methods: Antiproliferative activity of RO3280 was examined using the XTT assay. Flow cytometry assay was performed to evaluate cell cycle distribution, apoptosis, multicaspase activity, mitochondria' membrane potential, and DNA damage response. Apoptosis with fluorescence imaging studies was also examined. Results: According to the results of .XTT assay, although RO3280 displayed potent cytotoxicity in all treated cancer cells, the most sensitive cell line was identified as MCF-7 cells that were selected for further studies. The compound induced a cell cycle arrest in MCF-7 cells at G2/M phase and significantly induced apoptosis, multicaspase activity, DNA damage response, and decreased mitochondria' membrane potential of MCF-7 cells. Conclusion: Overall, RO3280 induces anticancer effects promoted mainly by DNA damage, cell cycle arrest, and apoptosis in breast cancer cells. Further studies are needed to assess its usability as an anticancer agent with specific cancer types.
dc.description.sponsorshipCumhuriyet University Scientific Research Project (CUBAP) [ECZ-045]
dc.description.sponsorshipThis study was supported by Cumhuriyet University Scientific Research Project (CUBAP, Project No: ECZ-045, Sivas, Turkey).
dc.identifier.doi10.2174/1871520619666190618162828
dc.identifier.endpage1854
dc.identifier.issn1871-5206
dc.identifier.issn1875-5992
dc.identifier.issue15
dc.identifier.pmid31244432
dc.identifier.scopus2-s2.0-85078577731
dc.identifier.scopusqualityQ3
dc.identifier.startpage1846
dc.identifier.urihttps://doi.org/10.2174/1871520619666190618162828
dc.identifier.urihttps://hdl.handle.net/20.500.12418/29417
dc.identifier.volume19
dc.identifier.wosWOS:000506818900006
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherBentham Science Publ Ltd
dc.relation.ispartofAnti-Cancer Agents in Medicinal Chemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectApoptosis
dc.subjectDNA damage
dc.subjectcell cycle
dc.subjectcytotoxicity
dc.subjectPLK inhibition
dc.subjectRO3280
dc.titleRO3280: A Novel PLK1 Inhibitor, Suppressed the Proliferation of MCF-7 Breast Cancer Cells Through the Induction of Cell Cycle Arrest at G2/M Point
dc.typeArticle

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