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Issue 11, 2017
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Selective inhibition of cancer cells by enzyme-induced gain of function of phosphorylated melittin analogues

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Abstract

The selective killing of cancer cells and the avoidance of drug resistance are still difficult challenges in cancer therapy. Here, we report a new strategy that uses enzyme-induced gain of function (EIGF) to regulate the structure and function of phosphorylated melittin analogues (MelAs). Original MelAs have the capacity to disrupt plasma membranes and induce cell death without selectivity. However, phosphorylation of Thr23 on one of the MelAs (MelA2-P) efficiently ameliorated the membrane lysis potency as well as the cytotoxicity for normal mammalian cells. After treatment with alkaline phosphatase (ALP), which is more active in cancer cells than normal cells, MelA2-P restored the pore-forming function around the cancer cells and induced cancer cell death selectively. This mechanism was independent of the receptor proteins and the cell uptake process, which may partially bypass the development of drug resistance in cancer cells.

Graphical abstract: Selective inhibition of cancer cells by enzyme-induced gain of function of phosphorylated melittin analogues

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Publication details

The article was received on 24 Jul 2017, accepted on 12 Sep 2017 and first published on 12 Sep 2017


Article type: Edge Article
DOI: 10.1039/C7SC03217J
Citation: Chem. Sci., 2017,8, 7675-7681
  • Open access: Creative Commons BY-NC license
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    Selective inhibition of cancer cells by enzyme-induced gain of function of phosphorylated melittin analogues

    Q. Li, P. Chen, Z. Hu, Y. Cao, L. Chen, Y. Chen, Y. Zhao and Y. Li, Chem. Sci., 2017, 8, 7675
    DOI: 10.1039/C7SC03217J

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