Radiofrequency field-induced thermal cytotoxicity in cancer cells treated with fluorescent nanoparticles.
BACKGROUND
Nonionizing radiation, such as radiofrequency field and near infrared laser, induces thermal cytotoxicity in cancer cells treated with gold nanoparticles. Quantum dots are fluorescent semiconducting nanoparticles that were hypothesized to induce similar injury after radiofrequency field irradiation.


METHODS
Gold nanoparticles and 2 types of quantum dot (cadmium-selenide and indium-gallium-phosphide) conjugated to cetuximab (C225), a monoclonal antibody against human epidermal growth factor receptor (EGFR)-1, demonstrated concentration-dependent heating in a radiofrequency field. The authors investigated the effect of radiofrequency field exposure after targeted nanoparticle treatment in a coculture of 2 human cancer cell lines that have differential EGFR-1 expression (a high-expressing pancreatic carcinoma, Panc-1, and a low-expressing breast carcinoma, Cama-1).


RESULTS
Radiofrequency revealed that Panc-1 or Cama-1 cells not containing gold nanoparticles or quantum dots had a viability of > 92%. The viability of Panc-1 cells exposed to the radiofrequency field after treatment with 50 nM Au-C225 was 39.4% +/- 8.3% without injury to bystander Cama-1 cells (viability was 93.7% +/- 1.0%; P approximately .0006). Panc-1 cells treated with targeted cadmium-selenide quantum dots were only 47.5% viable after radiofrequency field exposure (P< .0001 compared with radiofrequency only Panc-1 control cells). Targeted indium-gallium-phosphide quantum dots decreased Panc-1 viability to 58.2% +/- 3.4% after radiofrequency field exposure (P = approximately .0004 compared with Cama-1 and Panc-1 controls).


CONCLUSIONS
The authors selectively induced radiofrequency field cytotoxicity in Panc-1 cells without injury to bystander Cama-1 cells using EGFR-1-targeted nanoparticles, and demonstrated an interesting bifunctionality of fluorescent nanoparticles as agents for both cancer cell imaging and treatment.
Glazer
Evan S
ES
Department of Surgical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.
Curley
Steven A
SA
D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000008:administration & dosage*; D017209:Apoptosis; D000068818:Cetuximab; D016503:Drug Delivery Systems; D066246:ErbB Receptors / Q000276:immunology / Q000378:metabolism; D005453:Fluorescence; D006046:Gold / Q000493:pharmacokinetics; D006979:Hyperthermia, Induced / Q000379:methods*; D053768:Metal Nanoparticles; D010190:Pancreatic Neoplasms / Q000628:therapy*; D045663:Quantum Dots; D011846:Radio Waves
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D006046:Gold; D066246:ErbB Receptors; D000068818:Cetuximab