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Mitochondrial DNA (mtDNA) transcription is an emerging target in cancer therapy. While enzyme-targeted inhibitors like IMT1B block POLRMT, their organelle specificity remains unclear. Here, we report a distinct strategy using mitochondria-accumulating nonplanar perylene diimides (PDIs). We demonstrate that the fluorescent lead compound PDIC-BL selectively accumulates within mitochondria. Single-molecule stretching assays showed that PDIC-BL interacts with mtDNA-derived double-stranded DNA templates in vitro with an affinity comparable to ethidium (Kd = 32 μM). In cells, this mitochondrial accumulation and DNA-binding capability enable PDIC-BL to suppress mitochondrially encoded gene expression, thereby contributing to mitochondrial dysfunction, oxidative stress, and apoptosis-associated cell death. Consequently, PDIC-BL exhibits potent antitumor activity in breast cancer cell lines (MCF-7, MDA-MB-231) and significantly suppresses tumor growth in vivo, with preliminary tolerability in a cancer xenograft model in nude mice. This work offers a generalizable strategy for developing mitochondria-biased DNA-binding therapeutics.
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Huo et al. (2026) studied this question.
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