Peroxiredoxin 1 promotes tumorigenesis through regulating the activity of mTOR/p70S6K pathway in esophageal squamous cell carcinoma.

Abstract

The biological function of Peroxiredoxin 1 (Prdx1) in cancer is still ambiguous, and its mechanism has not been elucidated so far. Previous studies have shown that Prdx1 functions as tumor suppressor in several types of cancers, but other studies have indicated that it is overexpressed in some types of human cancers, and inhibition of Prdx1 by shRNA contributes to radiosensitivity and chemosensitivity. In this study, a suppression subtractive hybridization cDNA library between esophageal squamous cell carcinoma (ESCC) cell line EC9706 and noncancerous esophageal epithelial cell line Het-1A was constructed, and 11 tumorigenesis-associated genes including Prdx1 were isolated. In addition, we further confirmed that Prdx1 was overexpressed in ESCC cells at the level of protein compared with Het-1A (P<0.05). Inhibition of Prdx1 by shRNA lentivirus decreased cell proliferation and invasion, and induced cell apoptosis, but did not affect cell cycle distribution of EC9706 cells (P>0.05). Importantly, the total proteins of mTOR and p70S6K, as well as the activity of mTOR/p70S6K signaling pathway, were decreased in Prdx1-depletion EC9706 cells. Furthermore, the activity of mTOR/p70S6K signaling pathway was increased in Prdx1-overexpressing Het-1A cells. These findings mentioned above demonstrate that Prdx1 may be involved in tumorigenesis through regulation of mTOR/p70S6K pathway in ESCC.