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RNA microarray of human cervical cancer cell line HeLa treated with imatinib, mitoxantrone or mitoxantrone+imatinib combination against untreated controls

ABSTRACT: Critical DNA repair pathways become deranged during cancer development. This vulnerability may be exploited with DNA-targeting chemotherapy. Topoisomerase II inhibitors induce double-strand breaks which are detrimental to the cell, if not repaired. This repair process requires high-fidelity functional homologous recombination or error-prone non-homologous recombination. If either of these pathways is targeted, the compensatory pathway may rescue the cells and induce treatment resistance. c-Abl is a protein tyrosine kinase that is involved in cell differentiation, cell division, cell adhesion, and stress response including DNA damage induced stress. Here we used a low dose topoisomerase II inhibitor mitoxantrone to induce DNA damage and c-Abl kinase inhibitor imatinib in combination and studied the drug effects at transcriptomic level. The microarray data suggests that DNA repair, particularly homologous recombination, is downregulated together with alterations in cell cycle regulation. The data prompted to further validation assays on functional level which are shown in the original publication.

ORGANISM(S): Homo sapiens

SUBMITTER: Sakari Hietanen

PROVIDER: E-MTAB-9475 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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