PRDX2 removal inhibits the cell cycle and autophagy in colorectal cancer cells.

Aging
Xiangru ZhengZhongxue Fu

Abstract

Colorectal cancer (CRC) is a prevalent worldwide disease in which the antioxidant enzyme peroxiredoxin 2 (PRDX2) plays an important role. To investigate the molecular mechanism of PRDX2 in CRC, we performed bioinformatics analysis of The Cancer Genome Atlas (TCGA) datasets and Gene Expression Omnibus (GEO) DataSets (accession no. GSE81429). Our results suggest that PRDX2 is associated with cell-cycle progression and autophagy activated by the P38 MAPK/FOXO signaling pathway. Using a short-hairpin RNA vector, we verified that PRDX2 is essential for CRC cell proliferation and S-phase progression. Immunostaining, electron microscopy and western blotting assays verified the effect of PRDX2 knockdown on autophagy flux and p38 activation. The P38 activator dehydrocorydaline chloride partially rescued the effects of sh-PRDX2 on the expression of proteins related to cell-cycle progression and autophagy. We verified the correlation between PRDX2 expression and the expression of an array of cell-cycle and autophagy-related genes using data from an independent set of 222 CRC patient samples. A mouse xenoplast model was consistent with in vitro results. Our results suggest that PRDX2 promotes CRC cell-cycle progression via activation of th...Continue Reading

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Citations

Apr 4, 2021·Antioxidants·Lucie Valek, Irmgard Tegeder

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Datasets Mentioned

BETA
GSE81429

Methods Mentioned

BETA
RNA-seq
flow cytometry
transmission electron microscopy
transfection
xenografts

Software Mentioned

Bioconda
FastQC
ModFit
RStudio
clusterProfiler
Graph Pad Prism
SRA Toolkit
DESeq2

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