1 Ocak 2024 Dergi makalesi Açık Erişim

Asik, Aycan; Kara, Hale Guler; Ozates, Neslihan Pinar; Gunduz, Cumhur

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    <subfield code="a">&lt;p&gt;Objective: A relationship exists between breast cancer stem cells (BCSCs) and the chemo-resistance and recurrence of aggressive breast tumors. Amcasertib is a small chemical compound and multiple kinase inhibitor that inhibits downstream Nanog and other cancer stem signaling pathways in cancer stem cells by targeting several serine-threonine kinases. In this study, we aimed to investigate the cytotoxicity&lt;br&gt; and anticancer effects of Amcasertib on BCSCs, gaining insight into the targetability of BCSCs.&lt;br&gt; Method: We used the combined xCELLigence-Real-Time Cell Analyzer (RTCA) equipment to analyze cytotoxicity and cell proliferation. We detected the IC50 dosages of Amcasertib at 24, 48, and 72 hours and examined its effects on apoptosis, cell cycle, invasion, and migration over 48 hours. We used flow cytometry for assays of apoptosis and cell cycle, and the CytoSelect 96-well Cell Migration and Invasion Assay&lt;br&gt; Kit for evaluating invasion and migration.&lt;br&gt; Results: Our results showed that Amcasertib has cytotoxic properties, with an IC50 dosage of 1.9 mu M at the 48th hour. In addition, Amcasertib significantly induced apoptosis in BCSCs, despite not affecting the cell cycle. Moreover, Amcasertib decreased BCSCs' invasion and migratory properties, part of epithelial-mesenchymal transition (EMT).&lt;br&gt; Conclusion: In conclusion, our findings provide crucial information for understanding the potential of Amcasertib in targeting BCSCs. In addition, we suggest that Amcasertib could be a beneficial drug for breast cancer treatment by targeting BCSCs.&lt;/p&gt;</subfield>
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    <subfield code="a">Asik, Aycan</subfield>
    <subfield code="u">Mugla Sitki Kocman Univ, Fac Med, Dept Med Biol, Mugla, Turkiye</subfield>
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    <subfield code="a">Amcasertib Increases Apoptosis While Decreasing Invasive and Migrating Abilities in Breast Cancer Stem Cells</subfield>
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