Inhibition of STAT1 sensitizes radioresistant nasopharyngeal carcinoma cell line CNE-2R to radiotherapy
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Song Qu1,*, Ya Guo1,2,*, Shi-Ting Huang1 and Xiao-Dong Zhu1
1Department of Radiation Oncology, The Affiliated Tumor Hospital of Guangxi Medical University, Cancer Institute of Guangxi Zhuang Autonomous Region, Key Laboratory of High Incidence Tumor Prevention and Treatment Guangxi Medical University, Ministry of Education, Nanning, 530021, PR China
2Department of Oncology, The Second Affiliated Hospital of Medical School of Xi'an Jiao Tong University, Xi'an, Shanxi Province, 710004, PR China
*These authors contributed equally to this work and are co-first authors
Xiao-Dong Zhu, email: firstname.lastname@example.org
Keywords: nasopharyngeal carcinoma, radioresistance, signal transducer and activator of transcription 1(STAT1), lentivirus-mediated RNA interference
Received: September 28, 2016 Accepted: July 13, 2017 Published: July 29, 2017
Radioresistance remains a major obstacle for clinicians in the treatment of nasopharyngeal carcinoma (NPC). Others and we have reported that signal transducer and activator of transcription 1 (STAT1) may be as an important gene for resistance to radiation. However, the relationship between STAT1 and radioresistance is still elusive. In this study, by constitutive silencing STAT1 in human radioresistant nasopharyngeal carcinoma CNE-2R cell line, we showed that inhibition of STAT1 enhanced radiosensitivity of CNE-2R. Furthermore, knockdown of STAT1 led to growth suppression and apoptosis promotion in vitro and in vivo. Moreover, cells with low STAT1 expression increased G2/M phase and decreased S phase at 2Gy. These result revealed that knockdown of stat1 expression could sensitizes the CNE-2R to radiotherapy, But the exact mechanism needs to be further clarified.
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