Wenli Huang

Sichuan University, Hua-yang, Sichuan, China

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Publications (3)8.02 Total impact

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    ABSTRACT: Studies on the anticancer mechanism of peptide P18 in human leukemia K562 cells revealed that P18 causes the death of most K562 cells by depolarizing plasma membrane potential and enhancing membrane permeability, rather than activating the classical apoptosis pathway. The mechanistic studies indicate that disrupting plasma membrane is an effective approach to kill cancer cells and help design more effective peptide analogues in future cancer therapies.
    No preview · Article · Mar 2010 · Organic & Biomolecular Chemistry
  • Wenli Huang · Li Lu · Ximing Shao · Chengkang Tang · Xiaojun Zhao
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    ABSTRACT: The anticancer properties and mechanism of action of a hybrid peptide -P18 were investigated. It had significant cytotoxic activity against human melanoma cells and low toxicity to normal NIH-3T3 cells. It also induced cell death via necrosis rather than classical apoptosis. The peptide targets the cells membrane, causing a sustained depolarization of transmembrane potential resulting in the cells swelling and bursting, thereby triggering cytolysis. P18 peptide initially binds to the melanoma cell membrane via electrostatic interaction, causing the cell membrane to rupture. The effect may be mediated by the amphiphilic alpha-helical structure of P18 peptide, coupled with changes in ion channels and an increase in plasma membrane permeability that eventually leads to melanoma cell death.
    No preview · Article · Dec 2009 · Biotechnology Letters
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    ABSTRACT: Nanofiber scaffolds formed by self-assembling peptide RADA16-I have been used for the study of cell proliferation to mimic an extracellular matrix. In this study, we investigated the effect of RADA16-I on the growth of human leukemia cells in vitro and in nude mice. Self-assembly assessment showed that RADA16-I molecules have excellent self-assembling ability to form stable nanofibers. MTT assay displayed that RADA16-I has no cytotoxicity for leukemia cells and human umbilical vein endothelial cells (HUVECs) in vitro. However, RADA16-I inhibited the growth of K562 tumors in nude mice. Furthermore, we found RADA16-I inhibited vascular tube-formation by HUVECs in vitro. Our data suggested that nanofiber scaffolds formed by RADA16-I could change tumor microenvironments, and inhibit the growth of tumors. The study helps to encourage further design of self-assembling systems for cancer therapy.
    Preview · Article · Jun 2009 · International Journal of Molecular Sciences

Publication Stats

23 Citations
8.02 Total Impact Points


  • 2009
    • Sichuan University
      • Department of Thoracic and Cardiovascular Surgery
      Hua-yang, Sichuan, China