AI Article Synopsis
- A ruthenium(II) β-carboline complex, [Ru(tpy)(Nh)3](2+), was synthesized and found to selectively induce apoptosis in cancer cells while sparing normal cells.
- In mouse models, the complex significantly reduced tumor growth in MCF-7 and HepG2 cell lines.
- The mechanism involved the mitochondrial pathway, leading to p53 protein accumulation and activation of cell death proteins, indicating its potential for future cancer treatment advancements.
Article Abstract
A ruthenium(II) β-carboline complex [Ru(tpy)(Nh)3](2+) (tpy = 2,2':6',2″-terpyridine, Nh = Norharman, Ru1) has been synthesized and characterized. This complex induced apoptosis against various cancer cell lines and had high selectivity between tumor cells and normal cells. In vivo examination indicated Ru1 decreased mouse MCF-7 and HepG2 tumor growth. Signaling pathways analysis demonstrated that this complex induced apoptosis via the mitochondrial pathway, as evidenced by the loss of mitochondrial membrane potential (MMP, ΔΨm) and the release of cytochrome c. The resulting accumulation of p53 proteins from phosphorylation at Ser-15 and Ser-392 correlated with an increase in p21 and caspase activation. Taken together, these findings suggest that Ru1 exhibits high and selective cytotoxicity induced p53-mediated apoptosis and may contribute to the future development of improved chemotherapeutics against human cancers.
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| http://dx.doi.org/10.1016/j.biochi.2013.07.016 | DOI Listing |
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