Novel function of PERP-428 variants impacts lung cancer risk through the differential regulation of PTEN/MDM2/p53-mediated antioxidant activity

Lung cancer is the leading cause of cancer-related deaths worldwide. Identifying genetic risk factors and understanding their mechanisms will help reduce lung cancer incidence. The p53 apoptosis effect is related to PMP-22 (PERP), a tetraspan membrane protein, and an apoptotic effector protein downs...

Full description

Saved in:
Bibliographic Details
Published in:Free radical biology & medicine 2021-05, Vol.167, p.307-320
Main Authors: Liao, Chen-Yi, Yang, Shun-Fa, Wu, Ting-Jian, Chang, Han, Huang, Chi-Ying F., Liu, Yu-Fan, Wang, Chi-Hsiang, Liou, Jhong-Chio, Hsu, Shih-Lan, Lee, Huei, Sheu, Gwo-Tarng, Chang, Jinghua Tsai
Format: Article
Language:English
Subjects:
Antioxidants
Apoptosis
Catalase
Genes, Tumor Suppressor
Glutathione reductase
Humans
Lung Neoplasms - genetics
MDM2
Membrane Proteins
p53
PERP
Proto-Oncogene Proteins c-mdm2 - genetics
PTEN
PTEN Phosphohydrolase - genetics
SNP
Tumor Suppressor Protein p53 - genetics
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Lung cancer is the leading cause of cancer-related deaths worldwide. Identifying genetic risk factors and understanding their mechanisms will help reduce lung cancer incidence. The p53 apoptosis effect is related to PMP-22 (PERP), a tetraspan membrane protein, and an apoptotic effector protein downstream of p53. Although historically considered a tumor suppressor, PERP is highly expressed in lung cancers. Stable knockdown of PERP expression induces CL1-5 and A549 lung cancer cell death, but transient knockdown has no effect. Interestingly, relative to the PERP-428GG genotype, PERP-428CC was associated with the highest lung cancer risk (OR = 5.38; 95% CI = 2.12–13.65, p 
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2021.02.017