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Cellular Responses to Anthracyclines Identify Ku70, a DNA Repair Factor that Changes Compartment and Remains Stable in Leukemic Cells

Karima El Fadili, Emil Andreev, Zhiqiang Wang, Dindial Ramotar

Abstract


Anthracyclines such as doxorubicin and daunorubicin are anticancer drugs that act by damaging the DNA and used for treating a variety of cancers including adult acute myeloid leukemia. To date, nearly 50 % of acute myeloid leukemia patients show resistance to anthracyclines although the cause is not known. We first investigate if there is a relationship between the expression level of 23 DNA repair genes in three leukemic cell lines (KG-1, HL-60 and Mono-Mac1) and cellular responses to anthracyclines. We observed that the DNA repair genes were all downregulated in these cell lines following exposure to doxorubicin. Further analysis revealed that the general downregulation of the genes was linked to a substantial decrease in the recovery of total RNA raising the possibility that assessment of total RNA, and not specific gene or set of genes, can be used as a simple indicator of cellular responses to anthracyclines. Furthermore, examination of total protein extracts derived from these cell lines revealed for the first time that Ku70 is a key protein that remained stable, while the majority of proteins were loss, upon anthracycline treatment. Importantly, Ku70 redistributes from the cytoplasm to the nucleoli in a time-dependent manner in response to anthracycline exposure. We propose that Ku70 redistribution might play a vital role in predicting cellular response to anthracycline and promoting cell death.


Keywords


Ku70; Leukemia; Anthracyclines; Gene expression profile; DNA damage; Total RNA

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