BTG1 and Its Related Pathways in Cellular Response to X-ray and Carbon Ion Radiation

TIAN Ning; LI He; JIN Liangliang; HUA Junrui; MA Yingchun; HE Jinpeng; WU Xin; WANG Jufang

doi:10.11804/NuclPhysRev.33.04.481

BTG1, an important anti-proliferative gene, plays critical roles in cellular response to stresses, including ionizing radiation (IR). However, the long term expression of BTG1 induced by IR and its upstream/downstream signal pathways have not been elucidated clearly until now. The qRT-PCR results showed that the expression level of BTG1 in 786-O cells was rapidly elevated by IR in a short time, and then decreased slowly. In addition, upregulation or downregulation by transfection of BTG1 overexpression vector or siRNA could significantly affect the carbon ion radiation-induced genomic instability. Further study indicated that IRinduced BTG1 expression may be regulated by NF-B-mediated activation of SKA2 indirectly; On the other hand, expression of BTG1 may cause epigenetic changes by activating PRMT1, and subsequently influence the genomic stability, cell cycle regulation and apoptosis.

BTG1 and Its Related Pathways in Cellular Response to X-ray and Carbon Ion Radiation

1. School of Pharmacy, Lanzhou University, Lanzhou 730000, China;

2. Gansu Key Laboratory of Space Radiobiology, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China;

3. Lanzhou General Hospital, Lanzhou Command of CPLA, Lanzhou 730000, China

Funds: National Natural Science Foundation of China (U1232125, 31270895, 11405232)

Received Date: 2015-12-12

Rev Recd Date: 2016-02-09

Publish Date: 2016-12-20

Key words:

Ionizing radiation /
BTG1 /
NF-кB /
PRMT1 /
Epigenetics

Abstract: BTG1, an important anti-proliferative gene, plays critical roles in cellular response to stresses, including ionizing radiation (IR). However, the long term expression of BTG1 induced by IR and its upstream/downstream signal pathways have not been elucidated clearly until now. The qRT-PCR results showed that the expression level of BTG1 in 786-O cells was rapidly elevated by IR in a short time, and then decreased slowly. In addition, upregulation or downregulation by transfection of BTG1 overexpression vector or siRNA could significantly affect the carbon ion radiation-induced genomic instability. Further study indicated that IRinduced BTG1 expression may be regulated by NF-B-mediated activation of SKA2 indirectly; On the other hand, expression of BTG1 may cause epigenetic changes by activating PRMT1, and subsequently influence the genomic stability, cell cycle regulation and apoptosis.

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Reference (27)

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BTG1 and Its Related Pathways in Cellular Response to X-ray and Carbon Ion Radiation

doi: 10.11804/NuclPhysRev.33.04.481

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