Aurora B kinase inhibition intensifies cisplatin cytotoxicity in MCF7 breast cancer cells

Abstract

Aim: Cancer, a complex and multifaceted group of diseases, poses a formidable challenge to global health. Characterised by uncontrolled cell growth and proliferation, it manifests in diverse forms, each with unique biological traits. Understanding the complexity of cancer biology is essential for developing targeted therapeutic interventions. This research aimed to explore the impact of inhibiting Aurora B kinase with BI 831266 on the anticancer efficacy of cisplatin in MCF7 cells, contributing to our understanding of potential treatment strategies. Materials and Methods: Good Cell Culture Practices were conducted in this research, where MCF7 human breast cancer cells were used in order to assess the therapeutic potential of the BI 831266 and cisplatin combination. Regarding functional experiments, we employed in vitro cell proliferation assay, 2D clonogenic survival assay, 3D colony formation assay and wound-healing assay. To elucidate the molecular mechanism underlying the observed functional outcomes, SDS-PAGE and Western blotting experiments were additionally conducted. Results: Our findings uncovered a synergistic interaction between inhibiting Aurora B kinase and treating MCF7 cancer cells with cisplatin. The combined treatment significantly increased cisplatin's cytotoxicity, hindered cancer cell migration, and influenced apoptotic pathways, as evident from changes in key protein expressions. Conclusion: Our research emphasises the significance of targeting Aurora B kinase in order to enhance therapeutic responses of cisplatin in MCF7 breast cancer cells. The study contributes valuable insights into potential combination therapies, offering a more effective and targeted approach for treating breast cancer.