Anticancer activity of RAPTA-EA1 in triple-negative BRCA1 proficient breast cancer cells: single and combined treatment with the PARP inhibitor olaparib

We studied the anticancer activity of RAPTA-EA1 on triple-negative BRCA1 competent breast cancer MDA-MB-231 cells

Khwanjira Hongthong; Tidarat Nhukeaw; Pornvichai Temboot; Paul J. Dyson; Adisorn Ratanaphan


Scholarcy highlights

  • Breast cancer is a diverse disease and has been classified into biological subtypes with distinct histopathological, genetic and epigenetic characteristics
  • The cytotoxicity effect of RAPTA-EA1 on MDA-MB-231 breast cancer cells was performed by a MTT assays, using cisplatin as a control
  • This study provides further mechanistic insights on the mode of action of RAPTA-EA1, a ruthenium-based GSTP-1 inhibitor, for the treatment of triple-negative BRCA1-competent MDA-MB-231 breast cancer cells
  • RAPTA-EA1 induces an irreversible, anomalous state of condensed chromatin, rutheniumadducts in the specific nucleosome core, which blocks the binding of a key protein for nuclear factor association and chromatin condensation inducing alterations in chromatin fiber folding
  • This association generates substantial of mitotic cell death at the G2/M phase of the cell cycle progression
  • About 5 Â 106 MDA-MB-231 cells were incubated with RAPTA-EA1 at 37 C for 48 h under 5% CO2
  • The evidence suggests that cellular DNA damage triggers the inactivation of phosphorylation to cyclin-dependent kinase CDK1-cyclin B1 complex, which leads to cell death through G2/M checkpoint deregulation
  • It seems that drug susceptibility in triple-negative BRCA1 wildtype breast cancer MDA-MB-231 cells is linked to the reduced expression of the BRCA1 protein in repairing DNA damage after RAPTA-EA1 exposure

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