Bidirectional Regulation of MnSOD and Radiosensitivity of Esophageal Cancer Cells

Manganese superoxide dismutase (MnSOD) is a newly recognized anti-oncogene with low expression or detection in breast cancer (Soini et al., 2001), prostatic cancer (Wang et al., 2006), lung cancer (Zejnilovic et al., 2009), and esophageal cancer (Sun et al., 2011). Interestingly, the overexpression of MnSOD reduced metastasis rates (Wang et al., 2005) and inhibited or reversed the malignant phenotype of human fibroblast SV40 (Yan et al., 1996), malignant melanoma (Church et al., 1993)and neuroglioma (Zhong et al., 1997). However, we found that overexpression of MnSOD did not always inhibit tumor growth. High MnSOD overexpression inhibited the growth of SaOS2 osteosarcoma cells, producing low inoculation efficiency with a longer doubling time, whereas moderate overexpression produced high inoculation efficiency and a shorter doubling time (Wang et al., 2005). We speculated that by regulating the levels of MnSOD overexpression, in the presence of nitric oxide (NO) and adriamycin (ADR), would alter the types and concentrations of reactive oxygen species (ROS) and reaction products in a biodirectional manner (Wang et al., 2005). We previously showed that protein expression levels of MnSOD in esophageal carcinoma cells were 1Department of Chemoradiotherapy, Tangshan People’s Hospital, 4Department of Endocrinology, Tangshan Workers Hospital, Tangshan, 2Department of Radiotherapy, The Military General Hospital of Beijing PLA, Beijing, 3Department of Radiotherapy, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China *For correspondence: [email protected] Abstract