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

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.