Dp44mT is a potent iron chelator, which shows selective antitumor activity.
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Dp44mT is an iron chelator with selective anticancer activity. Dp44mT alone induced selective cell killing in the breast cancer cell line MDA-MB-231, due to selective inhibition of top2alpha, when compared with healthy mammary epithelial cells (MCF-12A). It induces G1 cell cycle arrest and reduces cancer cell clonogenic growth at nanomolar concentrations. Dp44mT, but not the iron chelator desferal, induces DNA double-strand breaks quantified as S139 phosphorylated histone foci (gamma-H2AX) and Comet tails induced in MDA-MB-231 cells. Doxorubicin-induced cytotoxicity and DNA damage were both enhanced significantly in the presence of low concentrations of Dp44mT. The chelator caused selective poisoning of DNA topoisomerase IIalpha (top2alpha) as measured by an in vitro DNA cleavage assay and cellular topoisomerase-DNA complex formation[3]. Dp44mT targets lysosome integrity through copper binding. Copper binding is essential for the potent antitumor activity of Dp44mT, as coincubation with nontoxic copper chelators markedly attenuated its cytotoxicity[4]. Dp44mT induces translocation of TFEB to the nucleus and it was AMPK-dependent[5].
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