Knockdown of hepatoma-derived growth factor-related protein-3 induces apoptosis of H1299 cells via ROS-dependent and p53-independent NF-kappa B activation
- Authors
- Yun, Hong Shik; Baek, Jeong-Hwa; Yim, Ji-Hye; Lee, Su-Jae; Lee, Chang-Woo; Song, Jie-Young; Um, Hong-Duck; Park, Jong Kuk; Park, In-Chul; Hwang, Sang-Gu
- Issue Date
- Jul-2014
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- H1299 cells; HRP-3; Myc/Noxa signaling; NF-kappa B; ROS
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.449, no.4, pp.471 - 476
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 449
- Number
- 4
- Start Page
- 471
- End Page
- 476
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/25843
- DOI
- 10.1016/j.bbrc.2014.05.039
- ISSN
- 0006-291X
- Abstract
- We previously identified hepatoma-derived growth factor-related protein-3 (HRP-3) as a radioresistant biomarker in p53 wild-type A549 cells and found that p53-dependent induction of the PUMA pathway was a critical event in regulating the radioresistant phenotype. Here, we found that HRP-3 knockdown regulates the radioresistance of p53-null H1299 cells through a distinctly different molecular mechanism. HRP-3 depletion was sufficient to cause apoptosis of H1299 cells by generating substantial levels of reactive oxygen species (ROS) through inhibition of the Nrf2/HO-1 antioxidant pathway. Subsequent, ROS-dependent and p53-independent NF-kappa B activation stimulated expression of c-Myc and Noxa proteins, thereby inducing the apoptotic machinery. Our results thus extend the range of targets for the development of new drugs to treat both p53 wild-type or p53-null radioresistant lung cancer cells. (C) 2014 The Authors. Published by Elsevier Inc.
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