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作 者:舒婷婷[1] 缪国英[2] 张红[3] 赵邱越[3] 卢启明[2]
机构地区:[1]兰州大学第一临床学院,甘肃兰州730000 [2]甘肃省人民医院,甘肃兰州730000 [3]中国科学院近代物理研究所,甘肃兰州730000
出 处:《现代生物医学进展》2016年第1期50-53,共4页Progress in Modern Biomedicine
基 金:甘肃省自然科学基金项目(096RJZA030)
摘 要:目的:利用不同剂量X射线对体外培养肝癌细胞HepG2进行照射,研究人宫颈癌基因(HCCR)及其相关基因对于细胞增殖的影响及其可能的分子机制。方法:采用0、1.0、2.0、4.0 Gy的吸收剂量X射线照射细胞,用克隆形成法观察细胞的存活情况;光镜下观察细胞形态变化;同时在辐照24 h后用RT-PCR法检测细胞中HCCR、p53、Bax mRNA的表达情况。结果:1.0、2.0、4.0 Gy吸收剂量时克隆形成率分别为(76.13±3.52)%、(62.22±2.17)%、(25.35±3.10)%,随着辐射剂量的增加细胞存活率显著下降(P<0.05)。HCCR mRNA相对表达量分别为0.95±0.04、0.8±0.07、0.45±0.03;p53 mRNA相对表达量分别为1.07±0.22、2.02±0.34、2.90±0.52;Bax mRNA相对表达量分别为1.12±0.11、1.63±0.36、2.48±0.27。较空白对照组,2Gy、4Gy剂量照射组HCCR mRNA相对表达量显著降低(P<0.05),而p53、Bax mRNA相对表达量显著增加(P<0.05)。结论:X射线照射可下调肝癌细胞HepG2的HCCR-1表达,抑制细胞增殖,作用机制可能与其相关基因p53、Bax表达升高有关。Objective: To study the effects and its possible molecular mechanisms of human cervical cancer oncogene-1 and its related genes on proliferation of HepG2 live cancer cells in vitro by using different doses of X-rays. Methods: By irradiating cancer cells with 0, 1.0, 2.0, 4.0 Gy of absorbed dose, the clonogenic assay was used to observe cell survival. Cell morphology changes was observed under Optical microscope. While the mRNA expression levels of HCCR, p53 and Bax were detected by RT-PCR. Results: Cloning efficiency rates of cells in 1.0, 2.0, 4.0 Gy of absorbed dose groups were(76.13 ±3.52)%,(62.22 ±2.17)%,(25.35 ± 3.10)%, respectively. As the radiation dose increased, cell viability decreased significantly(P〈0.05). The relative expression levels of HCCR mRNA amount were0.95 ± 0.04, 0.8 ± 0.07, 0.45 ± 0.03, respectively; The relative expression mRNA p53 were 1.07 ± 0.22, 2.02 ± 0.34, 2.90 ± 0.52;The relative expression mRNA Bax were 1.12 ± 0.11, 1.63 ± 0.36, 2.48 ± 0.27. Compared with the control group, 2Gy, 4Gy dose irradiation group HCCR-1 mRNA relative expression levels were significantly reduced(P〈0.05), but the relative expression levels of p53,Bax mRNA were significantly increased(P〈0.05). Conclusions: X-ray irradiation can downregulate HepG2 cancer cell HCCR relative expression levels and inhibit cell proliferation. The mechanism may be associated with gene p53, Bax expression elevated.
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