rmhTNF联合顺铂抑制人胃癌细胞增殖的作用机制  

The Mechanism of rmh TNF Combined with Cisplatin Inhibit the Proliferation of Human Gastric Cancer Cells

作　　者：袁明亮[1] 季万胜[2] 初国艳 林云[1] 杨丙信 高志星[2] 

机构地区：[1]潍坊医学院,山东潍坊261053 [2]潍坊医学院附属医院,山东潍坊261031 [3]利津县第二人民医院,山东东营257447

出　　处：《中国肿瘤》2015年第8期702-707,共6页China Cancer

基　　金：山东省优秀中青年科学家科研奖励基金(BS2010SW034)

摘　　要：[目的]探讨rmh TNF联合顺铂抑制人胃癌细胞增殖的作用机制。[方法]不同浓度rmh TNF(50,100,200IU/ml)单独或联合顺铂(4μg/ml)作用于人胃癌细胞系MKN45和SGC7901,细胞增殖/毒性检测试剂盒(CCK-8试剂盒)测定细胞抑制率;巢式逆转录多聚酶链反应(RT-PCR)测定细胞中p53β和caspase-3 m RNA的表达变化。[结果]CCK-8法结果显示,MKN45胃癌细胞中联合组细胞抑制率高于单独组,且随rmh TNF浓度的增加而增加,差异有统计学意义;而SGC7901胃癌细胞无此现象且单独rmh TNF对SGC7901胃癌细胞增殖抑制不明显,差异无统计学意义(F=1.01,P>0.05)。单独rmh TNF组中MKN45胃癌细胞抑制率随药物浓度增加而增加,差异有统计学意义(F=35.40,P<0.001)。RT-PCR结果显示,在MKN45胃癌细胞系中单独组和联合组caspase-3 m RNA表达均增加,且联合组均高于单独组并随rmh TNF浓度的增加而增加,组间差异有统计学意义(F=93.889,P<0.05);p53β在单独rmh TNF组中未见明显改变,差异无统计学意义(F=0.006,P>0.05),rmh TNF联合顺铂作用时可明显上调p53β的表达,并且随rmh TNF浓度的增加而增加,差异有统计学意义(F=18.577,P<0.001)。在SGC7901胃癌细胞中未见p53β表达;而caspase-3 m RNA的表达趋势与MKN45相同,组间差异有统计学意义(F=1409.656,P<0.05)。Person相关性分析显示,p53β与caspase-3表达呈正相关(r=0.766,P<0.001),细胞抑制率与caspase-3的表达呈正相关(r=0.978,P<0.001)。[结论]rmh TNF和顺铂对胃癌细胞系MKN45的协同抑制作用机制可能是通过p53β上调caspase-3。[Purpose] To investigate the mechanism of rmh TNF combined with cisplatin inhibit the proliferation of human gastric cancer cells. [Methods] Different concentrations rmh TNF（50,100,200IU/ml） alone or in combination with cisplatin（4μg/ml） was used intervene in human gastric cancer cell line SGC7901 and MNK45. the inhibition rate of gastric cancer cell lines was determined by cell proliferation/toxicity testing kits（CCK-8） assay. The change of p53β and caspase-3mRNA expression in MKN45 and SGC7901 were determined by Nested reverse transcription polymerase chain reaction（n RT-PCR）. [Results] CCK-8 assay showed that in MKN45 gastric cancer cell line the inhibition rate of monotherapy groups were higher than that in the combination groups,and with the increase of rmh TNF concentration increased,the difference was statistically significant,but there is no such phenomenon in SGC7901 gastric cancer cells and when different concentrations of rmh TNF intervene in it alone the cell proliferation inhibition was not obvious,the difference was not statistically significant（F=1.01,P〈0.05）. In MKN45 gastric cancer cells the inhibition rate of rmh TNF monotherapy groups with the increase of rmh TNF concentration increased,the difference was statistically significant（F =35.40,P〈0.001）. RT-PCR showed that in MKN45 gastric cancer cell lines the expression level of caspase-3 mRNA in monotherapy and combination groups were all increased and the combination groups were more than monotherapygroups and with the increase of rmh TNF concentration increased,the difference was statistically significant（F=93.889,P〈0.05）;p53β has no significant change in monotherapy groups of rmh TNF,the difference was not statistically significant（F=0.006,P〈0.05）.Combined intervention can significantly up regulated p53β and p53β increases with rmh TNF concentration,the difference was statistically significant（F=18.577,P〉0.001）. In SGC7901 gastric cancer cells the expression of p53βmRNA was not observed,the t

关 键 词：RMHTNF 顺铂 胃癌 p53β CASPASE-3 

分 类 号：R735.2[医药卫生—肿瘤]