Anti‐apoptotic role of peroxiredoxin III in cervical cancer cells

Abstract

As a member of peroxiredoxin (Prx) family, PrxIII is predominantly located in mitochondria and plays an important role as a scavenger of reactive oxygen species (ROS). Since previous reports demonstrated over-expression of PrxIII in cervical cancer, we conducted the present study to investigate the significance of PrxIII in cervical cancer development and/or progression.Cervical cancer cells were cultured from tissues derived from cervical cancer patients. After successful knockdown of PrxIII expression by small interfering RNA, we evaluated ROS level, viable cell number, and apoptosis of cervical cancer cells along with the culture time.The production of ROS was increased in cervical cancer cells as compared with normal cervical epithelia. Knockdown of PrxIII expression induced up-regulation of other Prx members including PrxI, PrxII, and PrxV. ROS level was higher in down-regulated cervical cancer cells than in controls and the difference was increasing with culture time. We also observed increased apoptosis and decreased viable cell number in down-regulated cervical cancer cells.Our results suggest that PrxIII is an indispensable ROS scavenger, which protects tumor cells against oxidative damage and subsequent apoptosis.

Peroxiredoxin proteins protect MCF-7 breast cancer cells from doxorubicin-induced toxicity

“…Prdx3 is a mitochondrial peroxiredoxin that is transcriptionally regulated by c-myc and is required for proliferation, transformation, and apoptosis in ovarian cancer cells (29). Recently, a similar function was reported for Prdx3 in cervical cancer cells (30). From these and other studies, the importance of Prdx3 as a key protective protein in cancer is well established.…”

The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells

“…Since most of chemotherapy for cancers is through increase in ROS level and apoptotic induction of cancer cells (Srinivas et al 2004;Alexandre et al 2006;Singh et al 2007;Brown et al 2010), some researchers have suggested PRX3 to be a potential target for cancer therapy on the basis of above fact Song et al 2011). Although the overlapping peroxidatic activities of PRXs contributed to drug resistance of cancer cells (Kalinina et al 2012), PRX3 played an indispensable role in apoptotic regulation (Chua et al 2010;Li et al 2013b;Whitaker et al 2013;Wang et al 2014;McDonald et al 2014). Therefore, we have reason to look forward to the desired effects by suppressing the expression of PRX3.…”

“…Because of active and indefinite growth of cancer cells, excessive ROS is produced in the cells, especially in mitochondria (Li et al 2013b;Tehan et al 2013). As an active responder to oxidative stress, PRX3 (or together with PRX5, another mitochondrial PRX gene) was significantly up-regulated in most common malignancies including breast cancer (Noh et al 2001;Karihtala et al 2003;Chua et al 2010), hepatocellular carcinoma (Choi et al 2002;Qiao et al 2012), malignant mesothelioma (MM) (Kinnula et al 2002), lung cancer Park et al 2006), cervical cancer (Kim et al 2009;Hu et al 2013), colorectal neoplasm (Wu et al 2010), prostate cancer (Basu et al 2011;Whitaker et al 2013), and endometrial cancer .…”

Peroxiredoxin 5 overexpression enhances tumorigenicity and correlates with poor prognosis in gastric cancer

“…Overexpression of PRXs in tumors have been suggested to be responsible for tumor progression, prognosis, and resistance to chemotherapy and radiotherapy (19,20). Overall, PRXs are peroxidases containing high antioxidant efficacy and are associated with cancer development and tumorigenesis in several kinds of cancer (21)(22)(23).…”

“…Lastly, PRXs are upregulated in various tumors in the breast, bladder, lung, cervical, ovarian, prostate, esophageal, and hepatocellular (19,(21)(22)(23). However, PRX expression and its impact on disease prognosis, patient survival rate, and EMT have rarely been studied in the context of human gastric cancer.…”