Communication

Gold Nanorods Mediate Tumor Cell Death by Compromising Membrane Integrity†

  1. L. Tong1,
  2. Y. Zhao1,
  3. T. B. Huff1,
  4. M. N. Hansen1,
  5. A. Wei1,
  6. J.-X. Cheng1,2

Article first published online: 17 OCT 2007

DOI: 10.1002/adma.200701974

Issue

Advanced Materials

Advanced Materials

Special Issue: Special Section on Bionanotechnology

Volume 19, Issue 20, pages 3136–3141, October, 2007

Additional Information

How to Cite

Tong, L., Zhao, Y., Huff, T. B., Hansen, M. N., Wei, A. and Cheng, J.-X. (2007), Gold Nanorods Mediate Tumor Cell Death by Compromising Membrane Integrity. Adv. Mater., 19: 3136–3141. doi: 10.1002/adma.200701974

Author Information

  1. 1

    Department of Chemistry, Purdue University, West Lafayette, IN 47907 (USA)

  2. 2

    Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907 (USA)

  1. †

    This work was supported by the National Institutes of Health (EB-001777), the National Science Foundation (CHE-0243496), and a grant from the Oncological Sciences Center at Purdue University. The authors thank Hongtao Chen for his assistance in SPT analysis, Professor Philip Low for providing folate-Bodipy and KB cells, and Professor Stephen Konieczny for providing NIH-3T3 cells. Supporting Information is available online from Wiley InterScience or from the authors.

Publication History

  1. Issue published online: 17 OCT 2007
  2. Article first published online: 17 OCT 2007
  3. Manuscript Received: 3 AUG 2007

Funded by

  • National Institutes of Health. Grant Number: EB-001777
  • National Science Foundation. Grant Number: CHE-0243496
  • Oncological Sciences Center at Purdue University

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Keywords:

  • Biomedical materials;
  • Bionanotechnology;
  • Inorganic nanorods;
  • Luminescence;
  • Membranes
Thumbnail image of graphical abstract

Folate-conjugated gold nanorods targeted to tumor cell surfaces produced severe membrane damage upon near-infrared irradiation. Photoinduced injury to the plasma membrane resulted in a rapid increase in intracellular calcium (shown in green) with subsequent disruption of the actin network, featured prominently by the formation of membrane blebs.

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