Reduced QSOX1 enhances radioresistance in nasopharyngeal carcinoma
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Lei Zhou1,*, Hong-Min Chen1,*, Song Qu1,2,3, Ling Li1,2,3, Wei Zhao1, Zhong-Guo Liang1, Bin-Bin Yu1, Kai-Hua Chen1, Qi-Teng Lu1, Guo-Xiang Lin1 and Xiao-Dong Zhu1,2,3,4
1Department of Radiation Oncology, Affiliated Tumor Hospital of Guangxi Medical University and Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, P.R. China
2Guangxi Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Guangxi Medical University, Nanning, Guangxi, P.R. China
3Key Laboratory of High-Incidence-Tumor Prevention and Treatment, Guangxi Medical University, Ministry of Education, Nanning, Guangxi, P.R. China
4Department of Oncology, Affiliated Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, P.R. China
*These authors contributed equally to this work
Xiao-Dong Zhu, email: [email protected]
Keywords: QSOX1; nasopharyngeal carcinoma; radiosensitivity; CNE-2; radiotherapy
Received: August 18, 2017 Accepted: November 16, 2017 Published: December 14, 2017
Radioresistance is a major cause leads to treatment failure in nasopharyngeal carcinoma (NPC). In our previous study, we identified that QSOX1 is a differentially expressed protein in NPC cell lines with variable radiosensitivities. The present study aimed to investigate the biological behavior of QSOX1 in nasopharyngeal carcinoma (NPC) and its effect on radiosensitivity. The levels of QSOX1 detected by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC) in radioresistant NPC patient sera and tissue samples were markedly lower than those in radiosensitive samples. Small hairpin RNAs (shRNAs) were employed to knock down endogenous QSOX1 expression in CNE-2 cells, and then, radiosensitivity, apoptosis, migration and invasion were assessed using colony formation, Cell Counting Kit-8 (CCK-8), flow cytometry, and transwell assays, respectively. Tumor growth and radioresistance were also evaluated using a xenograft model in nude mice. The shRNA-mediated knockdown of QSOX1 significantly increased cell survival under irradiation (IR) and weakened radiosensitivity, which was likely due to a reduction in the cell apoptosis rate after IR. Moreover, QSOX1 silencing led to the suppression of cellular migration and invasion. Similar results were obtained with the xenograft mouse model. Thus, targeting QSOX1 will provide a new avenue for increasing the sensitivity of NPC to radiotherapy.
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