As a common Redox, peroxiredoxin 3 (PRDX3) reportedly plays a significant role in regulating malignant tumor occurrence and development. However, the specific biological function and clinical roles remain unclear. Hence, we systematically investigated the correlation of PRDX3 with gene alteration and mutation, methylation, function, location, signaling pathways, tumor microenvironment, immune infiltration, and clinical prognosis in cancers using PRDX3 gene expression profiling, gene alterations, copy number variation, and clinical information of 33 types of cancers from The Cancer Genome Atlas. We further validated the biological role of PRDX3 in kidney clear cell carcinoma (KIRC) using reverse-transcription quantitative polymerase chain reaction, Western blot, Transwell and scratch assays. Generally, PRDX3 gene is differentially expressed in human malignant tumors, and its expression level may be regulated by gene copy number variation and methylation level. The PRDX3 gene expression level is closely related to the prognosis of cancer patients and plays dual roles. PRDX3 may regulate tumor progression by affecting tumor cell division, metabolism, REDOX processes, the tumor microenvironment and anti-tumor immune response in the body. In vitro experiments show that PRDX3 can inhibit the progression of KIRC cells by regulating the peroxisome proliferator-activated receptor signaling pathway. Studies targeting PRDX3 will promote the progress of tumor mechanism research, optimize tumor treatment, and ultimately improve the long-term prognosis of tumor patients.
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Chen et al. (2024) studied this question.
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