Overexpression of the immediate early response 5 gene increases the radiosensitivity of HeLa cells

The effects of the immediate early response 5 ( ) gene on the sensitivity of HeLa cells to radiation remain unclear. In the present study, stably transfected HeLa cells resulting in the knockdown or overexpression of were investigated. In addition, xenografts of normal, -silenced and -overexpressed...

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Published inExperimental and therapeutic medicine Vol. 18; no. 3; pp. 2704 - 2711
Main Authors Ding, Ku-Ke, Yang, Fen, Jiang, Hui-Qing, Yuan, Zeng-Qiang, Yin, Ling-Ling, Dong, Ling-Yue, Cui, Wei, Gou, Qiao, Liu, Xiao-Dan, Wu, Yu-Mei, Jiang, Xiao-Yan, Zhang, Xin, Zhou, Ping-Kun, Yang, Chuan-Jie
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.09.2019
Spandidos Publications UK Ltd
D.A. Spandidos
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Summary:The effects of the immediate early response 5 ( ) gene on the sensitivity of HeLa cells to radiation remain unclear. In the present study, stably transfected HeLa cells resulting in the knockdown or overexpression of were investigated. In addition, xenografts of normal, -silenced and -overexpressed HeLa cells were injected into nude mice and examined. The results demonstrated that the radiosensitivity of the -overexpressed HeLa cells was significantly increased compared with that of the normal and -silenced cells. The upregulation of effectively decreased cell proliferation and silencing promoted cell proliferation compared with that in the normal HeLa cells. Following irradiation of the cells with knockdown, cell cycle was arrested at the G /M phase and an increase in the proportion of S phase cells was observed. By contrast, the overexpression of 5 led to an increase in the proportion of G phase cells. Furthermore, the upregulation of inhibited tumor growth . The present findings demonstrate that the gene affects the radiosensitivity of HeLa cells and serves an important role in cell proliferation, suggesting that this gene may be a potential radiotherapeutic target in cervical cancer.
ISSN:1792-1074
1792-0981
1792-1082
DOI:10.3892/ol.2019.10590