Overexpression of the Peroxiredoxin V Inhibits the Picrasma quassioides Extract Induced Apoptosis in SiHa Cervical Cancer Cells
XIAO Wanqiu#, ZHANG Huina#, REN Chenxi, GUO Xiaoyu, LI Nan, CONG Jie, FENG Yaoyuan, SUN Hunan*
In recent years, traditional Chinese medicine treatments for cervical cancer have received more attentions due to their low toxicity and high efficiency. Prx V (Peroxiredoxin V), a major member of the Prxs (Peroxiredoxins) protein family, plays an important role in regulating the oxidative stress-induced cancer cell proliferation, migration, colony formation and apoptosis. The present study focused on the regulatory role of Prx V on PQE (Picrasma quassioides extract) induced apoptosis of human cervical cancer cells (SiHa cells), by constructing Mock and Prx V overexpressed SiHa cell lines. The cell viability, proliferation, migration, community formation, mitochondrial damage, apoptosis, intracellular ROS (reactive oxygen species) and apoptosis related protein expressions were investigated by MTT assay, scrape assay, colony formation assay, fluorescence micrography and Western blot. The results showed that PQE effectively increased intracellular ROS accumulation and induced apoptosis of SiHa cells by down-regulating the Prx V protein expression. In addition, overexpression of Prx V significantly reduced the PQE mediated intracellular ROS accumulations and apoptosis as well as the apoptosis-related proteins expression. These findings revealed that Prx V plays a protective role in PQE-induced apoptosis of cervical cancer SiHa cells, which provides a theoretical basis for exploring the clinical treatment strategy and the function of Prx V in cervical cancer.
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