About this Journal Submit a Manuscript Table of Contents
Journal of Oncology
Volume 2009 (2009), Article ID 780874, 9 pages
http://dx.doi.org/10.1155/2009/780874
Research Article

AP-2 Inhibits c-MYC Induced Oxidative Stress and Apoptosis in HaCaT Human Keratinocytes

1Free Radical & Radiation Biology Graduate Program, Radiation Oncology Department, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USA
2Department of Microbiology, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USA

Received 11 June 2009; Accepted 2 October 2009

Academic Editor: Jörg Kleeff

Copyright © 2009 Lei Yu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplemental Figure 1. Overexpression of AP-2α increased HaCaT cell survival rate upon UVA irradiation. HaCaT cells were infected with 100 MOI Ad-Bgl II or Ad-AP-2α for 24 hours. The cells then received 5 J per cm2 UVA irradiation. 100 cells were seeded immediately after UVA irradiation per plate. Clones that contained more than 50 cells were counted 2 weeks later. The survival rate of Bgl II control group was set arbitrarily to 100%. Error bars stands for SD, n=3.

Supplemental Figure 2. Overexpression c-MYC protein caused decreasing of AP-2α DNA binding activity. HaCaT cells were infected with increasing MOI of Ad-c-MYC. 24 hours later, the nuclear protein was extracted and 40 μg was analyzed with western blot and 5 μg was analyzed with gel shift assay. AP-2α DNA binding activity decreased while c-MYC protein levels increased. AP-2α protein level also showed no significant increased after c-MYC infection.

  1. Supplementary Figures