Published online Oct 14, 2015. doi: 10.3748/wjg.v21.i38.10840
Peer-review started: April 22, 2015
First decision: June 19, 2015
Revised: July 2, 2015
Accepted: August 31, 2015
Article in press: August 31, 2015
Published online: October 14, 2015
Processing time: 175 Days and 20.1 Hours
AIM: To investigate the expression characteristics of peroxiredoxin 1 (PRDX1) mRNA and protein in liver cancer cell lines and tissues.
METHODS: The RNA sequencing data from 374 patients with liver cancer were obtained from The Cancer Genome Atlas. The expression and clinical characteristics of PRDX1 mRNA were analyzed in this dataset. The Kaplan-Meier and Cox regression survival analysis was performed to determine the relationship between PRDX1 levels and patient survival. Subcellular fractionation and Western blotting were used to demonstrate the expression of PRDX1 protein in six liver cancer cell lines and 29 paired fresh tissue specimens. After bioinformatics prediction, a putative post-translational modification form of PRDX1 was observed using immunofluorescence under confocal microscopy and immunoprecipitation analysis in liver cancer cells.
RESULTS: The mRNA of PRDX1 gene was upregulated about 1.3-fold in tumor tissue compared with the adjacent non-tumor control (P = 0.005). Its abundance was significantly higher in men than women (P < 0.001). High levels of PRDX1 mRNA were associated with a shorter overall survival time (P = 0.04) but not with recurrence-free survival. The Cox regression analysis demonstrated that patients with high PRDX1 mRNA showed about 1.9-fold increase of risk for death (P = 0.03). In liver cancer cells, PRDX1 protein was strongly expressed with multiple different bands. PRDX1 in the cytosol fraction existed near the theoretical molecular weight, whereas two higher molecular weight bands were present in the membrane/organelle and nuclear fractions. Importantly, the theoretical PRDX1 band was increased, whereas the high molecular weight form was decreased in tumor tissues. Subsequent experiments revealed that the high molecular weight bands of PRDX1 might result from the post-translational modification by small ubiquitin-like modifier-1 (SUMO1).
CONCLUSION: PRDX1 was overexpressed in the tumor tissues of liver cancer and served as an independent poor prognostic factor for overall survival. PRDX1 can be modified by SUMO to play specific roles in hepatocarcinogenesis.
Core tip: Peroxiredoxin 1 (PRDX1) is an antioxidant enzyme, and, therefore, it is considered a tumor suppressor gene. However, only recently has various data revealed that PRDX1 not only functions in peroxide detoxification but also in tumorigenesis. Here, we found that PRDX1 was overexpressed in liver cancer at the transcriptional level, and it was an independent unfavorable prognostic factor for overall survival. In liver cancer cells, PRDX1 is post-translationally modified by small ubiquitin-like modifier. The downregulation of sumoylated PRDX1 in tumors might participate in hepatocarcinogenesis. PRDX1 represents both a prognostic biomarker and therapeutic target for liver cancer.