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©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Dec 10, 2014; 5(5): 1068-1077
Published online Dec 10, 2014. doi: 10.5306/wjco.v5.i5.1068
Published online Dec 10, 2014. doi: 10.5306/wjco.v5.i5.1068
MiR-210 expression reverses radioresistance of stem-like cells of oesophageal squamous cell carcinoma
Xin Chen, Jia Guo, Ru-Xing Xi, Yu-Wei Chang, Xiao-Zhi Zhang, Radiation Department, First Affiliated Hospital of Medical School of Xi’an Jiaotong University, Xi’an 710061, Shaanxi Provence, China
Fei-Yang Pan, School of Medicine, Queen’s University, Kingston K7L 3N6, Ontario, Canada
Author contributions: Chen X performed the majority of the experiments and analysed the data as well as wrote the manuscript; Xi RX collected the human tissues and the patients’ data; Guo J and Chang YW were both involved in cell culture, transfection, PCR and WB; Pan FY and Zhang XZ designed the experiments and amended the manuscript.
Supported by National Natural Science Foundation of China, No. 30972962
Correspondence to: Xiao-Zhi Zhang, Professor, MD, PhD, Chief Physician and Doctoral Tutor, Radiation Department, First Affiliated Hospital of Medical School of Xi’an Jiaotong University, West Yanta St., Xi’an 710061, Shaanxi Provence, China. zhang9149@sina.com
Telephone: +86-29-85324068 Fax: +86-29-85324068
Received: March 17, 2014
Revised: June 3, 2014
Accepted: August 27, 2014
Published online: December 10, 2014
Processing time: 268 Days and 15.5 Hours
Revised: June 3, 2014
Accepted: August 27, 2014
Published online: December 10, 2014
Processing time: 268 Days and 15.5 Hours
Core Tip
Core tip: A low level of miR-210 expression, which is common in oesophageal squamous cell carcinoma (ESCC) tissues, was found to be negatively correlated with the tumour pathological type and the prognosis in ESCC patients after radiotherapy, although the sample size was small. A relatively high level of in vitro miR-210 expression reversed the radioresistance of ESCC stem-like cells by decreasing the extent of ataxia telangiectasia mutated/DNA dependent protein kinase-dependent cell cycle arrest, failure of DNA double-strand break repair and stem cell proliferation.