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miR-21 regulates the radiation resistance of glioblastoma cells by inhibiting its target gene PDCD4 and hMSH2
CHAO Tengfei 1 #,XIONG Huihua 1,LIU Wei 2,CHEN Yang 3,ZHANG Jiaxuan 4 *
1.Cancer Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
2.Department of Neurosurgery, Beijing Tiantan Hospital,Capital Medical University, Beijing 100050, China
3.MOE Key Laboratory of Bioinformatics, Bioinformatics Division/Center for Synthetic & Systems Biology, TNLIST, Tsinghua University, Beijing 100084, China
4.Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
*Correspondence author
#Submitted by
Subject:
Funding: National Natural Science Foundation of China （No.No. 81201820, 81101691)）, Specialized Research Fund for the Doctoral Program of Higher Education （No.No. 20100142120041）
Opened online:26 September 2013
Accepted by: none
Citation: CHAO Tengfei,XIONG Huihua,LIU Wei.miR-21 regulates the radiation resistance of glioblastoma cells by inhibiting its target gene PDCD4 and hMSH2[OL]. [26 September 2013] http://en.paper.edu.cn/en_releasepaper/content/4560409
 
 
The purpose of this study was to investigate the molecular mechanism by which miR-21 and its target genes mediate radiation resistance of glioblastoma cells. Real-time PCR was employed to de-tect miR-21 expression in normal brain tissues, glioblastoma tissues and glioblastoma cell lines (A172, T98G and U87MG). T98G cells were transfected with anti-miR-21 oligonucleotides, or plasmids con-taining PDCD4 or hMSH2 (PDCD4-pcDNA3 and hMSH2-pcDNA3). The survival curve was obtained to investigate the sensitivity of T98G cells to radiation. Cell apoptosis was measured by using the Cas-pase-3/7 kit and cell cycle by flow cytometry. Western blotting was performed to detect the expression of hMSH2 and PDCD4 in miR-21-inhibiting T98G cells. The results showed that miR-21 expression in glioblastoma cells and tissues was conversely associated with the radiation sensitivity. Over-expression of miR-21 resulted in radiation resistance, while knockdown of miR-21 led to higher sensitivity of glioblastma cells to radiation. After miR-21 knockdown, the apoptosis of T98Gcells was significantly increased and the G2phase arrest was more significant. Inaddition, miR-21 knockdown increased the expression of endogenous PDCD4 and hMSH2, which contributed to the apoptosis and G2arrest of T98G cells. The findings suggested that miR-21 may mediate the resistance of glioblastoma cells against radiation via its target genes PDCD4 and hMSH2. MiR-21 and its target genes may be used as potential molecular targets for clinical radiotherapy sensitization in the future.
Keywords:microRNA; glioblastoma; radiation resistance
 
 
 

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