Ma Jianxun, Ye Lanping, Da Mingxu, Wang Xiaopeng
Department of General Surgery, The Peoples Hospital of Gansu Province, Lanzhou, People's Republic of China.
Mol Cell Biochem. 2009 Aug;328(1-2):17-23. doi: 10.1007/s11010-009-0069-6. Epub 2009 Mar 13.
The impact of STAT-3 expression on the apoptosis of human hepatomas cell SMMC-7721 line induced by X-ray and carbon ion irradiations was investigated.
Human hepatoma SMMC-7721 cells were irradiated with a carbon ion beam and X-ray. Cell survival was determined by a standard colony-forming assay. STAT-3 protein expression was analysed by Western Immunoblots. Cell cycle and apoptosis were performed by flow cytometry.
The viability of SMMC-7721 cells decreased with increasing dose of the carbon ion beam, and the high-LET carbon ion beam led to the cells getting arrested at G(2)/M phase. Western Blot analyses show that STAT-3 expression increased with increasing radiation dose. The carbon ion irradiation induced cell apoptosis and significantly promoted the expression of STAT-3 gene compared with the X-ray irradiation. The apoptosis rate is correlated with the expression of STAT-3 in human hepatoma SMMC-7721 cells after exposure to different doses of X-ray and heavy ion beam.
Heavy ion irradiation increases the expression of STAT-3 gene, makes SMMC-7721 cells arrested at G(2)/M phase and increases cell apoptosis in comparison with that induced by low-LET X-ray. The STAT-3 expression may be regarded as a protected reaction when the cancerous cells suffer a strong stimulus such as high-LET irradiation. The interaction of STAT-3 expression and other cytokines in human hepatoma and the relationship between STAT-3 and radiation-induced apoptosis remain to be clarified in the future.
研究STAT-3表达对X射线和碳离子辐射诱导的人肝癌细胞SMMC-7721系凋亡的影响。
用碳离子束和X射线照射人肝癌SMMC-7721细胞。通过标准集落形成试验测定细胞存活率。通过蛋白质免疫印迹分析STAT-3蛋白表达。通过流式细胞术检测细胞周期和凋亡。
SMMC-7721细胞的活力随碳离子束剂量增加而降低,高传能线密度碳离子束导致细胞停滞于G(2)/M期。蛋白质免疫印迹分析显示,STAT-3表达随辐射剂量增加而升高。与X射线照射相比,碳离子照射诱导细胞凋亡并显著促进STAT-3基因的表达。暴露于不同剂量X射线和重离子束后,人肝癌SMMC-7721细胞的凋亡率与STAT-3的表达相关。
与低传能线密度X射线相比,重离子照射增加STAT-3基因表达,使SMMC-7721细胞停滞于G(2)/M期并增加细胞凋亡。当癌细胞受到高传能线密度照射等强烈刺激时,STAT-3表达可能被视为一种保护反应。人肝癌中STAT-3表达与其他细胞因子的相互作用以及STAT-3与辐射诱导凋亡之间的关系尚待进一步阐明。