Peroxireduxin-4 is Over-Expressed in Colon Cancer and its Down-Regulation Leads to Apoptosis

Abstract

The objective of this study was to gain insight into the biological basis of colon cancer progression by characterizing gene expression differences between normal colon epithelium, corresponding colorectal primary tumors and metastases. We found a close similarity in gene expression patterns between primary tumors and metastases, indicating a correlation between gene expression and morphological characteristics. PRDX4 was identified as highly expressed both in primary colon tumors and metastases, and selected for further characterization. Our study revealed that "Prdx4" (PrxIV, AOE372) shows functional similarities to other Prx family members by negatively affecting apoptosis induction in tumor cells. In addition, our study links Prdx4 with Hif-1α, a key regulatory factor of angiogenesis. Targeting Prdx4 may be an attractive approach in cancer therapy, as its inhibition is expected to lead to induction of apoptosis and blockage of Hif-1α-mediated tumor angiogenesis.

Gamma-tocotrienol treatment increased peroxiredoxin-4 expression in HepG2 liver cancer cell line

“…NF-κB activation usually ensures cell proliferation and cell survival. Prx4 may prevent H 2 O 2 -induced activation of NF-κB by reducing H 2 O 2 [ 28 , 40 ]. By relating the antioxidant activity of Prx4 and the ability of NF-κB suppression by GTT, it is possible that Prx4 might indirectly help in suppressing NF-κB activation through H 2 O 2 metabolism.…”