Xu Zumin,Wang Jin,Zuo Yufang,Yu Zhonghua,Peng Fang,Hu Xiao,Zhou Qichao,Ma Honglian,Bao Yong,Chen Ming.Regulator of G-protein signaling 5 (RGS5) inhibits cell proliferation and enhances radiosensitivity of human lung cancer cells[J].Chinese Journal of Radiological Medicine and Protection,2014,34(11):803-808
Regulator of G-protein signaling 5 (RGS5) inhibits cell proliferation and enhances radiosensitivity of human lung cancer cells
Received:November 03, 2013  
DOI:10.3760/cma.j.issn.0254-5098.2014.11.002
KeyWords:Regulator of G-protein signaling 5  Lung cancer  Cell apoptosis  Radiation therapy
FundProject:国家自然科学基金(30872974,81172116,81201736);广东省科技计划项目(2009B030801154)
Author NameAffiliationE-mail
Xu Zumin Department of Radiation Oncology, Guangzhou 510060, China  
Wang Jin Sun Yat-Sen University Cancer Center, Guangzhou 510060, China  
Zuo Yufang State Key Laboratory of Oncology in South China, Guangzhou 510060, China  
Yu Zhonghua State Key Laboratory of Oncology in South China, Guangzhou 510060, China  
Peng Fang Department of Radiation Oncology, Guangzhou 510060, China  
Hu Xiao Department of Radiation Oncology, Guangzhou 510060, China  
Zhou Qichao Department of Radiation Oncology, Guangzhou 510060, China  
Ma Honglian Sun Yat-Sen University Cancer Center, Guangzhou 510060, China  
Bao Yong Department of Radiation Oncology, Guangzhou 510060, China  
Chen Ming Department of Radiation Oncology, Guangzhou 510060, China chenmingdr@zjcc.org.cn 
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Abstract::
      Objective To investigate the effects of regulator and the underlying molecular mechanisms of G-protein signaling 5 (RGS5) on radiation response in human lung cancer cells. Methods The effects of RGS5 on viability were determined by MTT assay, and apoptosis rate was detected by flow cytometry, in human lung cancer cells. The combined effect of ionizing radiation and RGS5 on tumor cells was detected by colony formation assay. The protein expression was detected by Western blot. Results RGS5 overexpression remarkably inhibited the survival of human lung cancer cells, and the growth inhibition rate of RGS5 overexpression on A549 and Calu-3 cells were 44.4% (F=29.18, P<0.05) and 39.27% (F=23.04, P<0.05) at 48 h, and 54.3%(F=103.45, P<0.05), 44.7%(F=108.02, P<0.05) at 72 h post-irradiation, respectively. RGS5 might exert its inhibitory effects on human lung cancer cells by inducing tumor cell apoptosis, while the apoptotic cells rate in A549 and Calu-3 cells in control group, pTRiEX group and pTRiEX-RGS5 group were (1.3±0.2)%, (3.4±0.6)%, (19.6±2.3)% (F=86.62,P<0.05), and (3.2±0.8)%, (3.0±0.9)%, (12.8±1.8)% (F=28.80,P<0.05) at 36 h post-irradiation, respectively. Furthermore, RGS5 could sensitize the lung cancer cells to radiation. Conclusions RGS5 might play an inhibitory role in human lung cancer cell proliferation, which may explain the pathoclinical observation thet high expression of RGSS is a favorable prognostic factor in NSCLC patients. In addition, RGS5 also enhance the anti-tumor effects of radiation in human lung cancer cells.
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