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BTG1是重要的抗细胞增殖蛋白,在细胞对外界胁迫如电离辐射等的应激响应过程中发挥重要功能。到目前为止,电离辐射诱导BTG1蛋白表达水平的长期变化情况、其对细胞基因组稳定性的影响及上下游相关的信号通路仍未完全阐明。通过荧光定量PCR技术发现BTG1对X射线和碳离子的应激呈现出先迅速升高再缓慢下降的过程。此外,微核实验表明,通过转染基因的质粒过表达载体或si RNA的方法外源性增加或抑制786-O细胞内BTG1的表达水平均能够显著影响碳离子辐照诱导的基因组不稳定性。深入研究发现电离辐射诱导的NF-κB的表达和活化可能通过引起SKA2基因的表达而间接地调控BTG1的表达,而BTG1则可能激活PRMT1的活性而引起基因组表观遗传学的改变,进而影响细胞的基因组稳定性、细胞周期调控以及凋亡等进程。
BTG1 is an important anti-cell proliferation protein that plays an important role in the stress response of cells to external stresses such as ionizing radiation. Up to now, the long-term changes of BTG1 protein expression induced by ionizing radiation have not fully elucidated the influence of cell genome stability and upstream and downstream signaling pathways. Fluorescence quantitative PCR showed that the stress of X-ray and carbon ion of BTG1 showed the first rapid increase and then the slow decrease. In addition, micronucleus experiments showed that exogenous increase or inhibition of BTG1 expression level in 786-O cells can significantly affect the genomic instability induced by carbon ion irradiation by plasmid transfection of plasmid overexpression vector or si RNA . In-depth study found that ionizing radiation-induced NF-κB expression and activation may indirectly by regulating the expression of SKA2 gene BTG1 expression, while BTG1 may activate the activity of PRMT1 cause genomic epigenetic changes, thereby affecting the cells The stability of the genome, cell cycle regulation and apoptosis.