期刊论文详细信息
Radiation Oncology
Overexpression of miRNA-21 promotes radiation-resistance of non-small cell lung cancer
Luo Jian-Chao3  Tan Xiao-Gang2  Zhao Jing3  Zhang Zhu-Bo1  Wang Wei3  Wang Xiao-chun1 
[1] Tianjin Key Laboratory of Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Science, Tianjin 300192, China;Department of Thoracic Surgery, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100021, China;Department of Radiation Oncology, Henan People’s Hospital, Henan 450003, China
关键词: Prognosis;    Radiation-resistancet;    NSCLC;    miRNA-21;   
Others  :  1153747
DOI  :  10.1186/1748-717X-8-146
 received in 2013-03-04, accepted in 2013-06-08,  发布年份 2013
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【 摘 要 】

Background

MiRNA-21 was previously reported to be up-regulated in many kinds of cancer. In the present study, we want to investigate the potential role of miRNA-21 in non-small cell lung cancer.

Materials and methods

Expression of miRNA-21 was detected in 60 non-small cell lung cancer (NSCLC) samples and adjacent histologically normal tissue using RT-qPCR, Correlation between miRNA-21 expression and clinicopathological features of NSCLC was analyzed using statistical software. The effect of miRNA-21 expression on the growth and apoptosis of A549 cells induced by irradiation was examined.

Results

miRNA-21 expression increased in non-small cell lung cancer. Expression of miRNA-21 was positively associated with lymph node metastasis, clinical stage and poor prognosis. Multivariate Cox regression analysis showed that miRNA-21 was an independent prognostic factor for patients. Down-regulation of miRNA-21 inhibited proliferation and cell cycle progress of A549 cells and sensitized cells to radiation. Decreased miRNA-21 expression promoted the apoptosis of A549 cells induced by irradiation.

Conclusions

miRNA-21 may be considered as a potential novel target for future development of specific therapeutic interventions in NSCLC.

【 授权许可】

   
2013 Xiao-chun et al.; licensee BioMed Central Ltd.

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