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作 者:崔璨[1] 葛振宇[2] 魏菁琳 张丽[2] 王春芽 张红梅[2] 季万胜[2] CUI Can1, GE Zhen-yu2, WEI Jing-lin1, et al.(1.Weifang Medical College, Weifang 261053 ,China;2. Affiliated Hospital of Weifang Medical College, Weifang 261031, Chin)
机构地区:[1]潍坊医学院,山东潍坊260153 [2]潍坊医学院附属医院.山东潍坊261031
出 处:《肿瘤学杂志》2018年第2期86-90,共5页Journal of Chinese Oncology
基 金:山东省优秀中青年科学家科研奖励基金(BS2010SW034)
摘 要:[目的]研究rmhTNF对胃癌细胞系MKN45的生物学效应及其机制。[方法]采用不同浓度(50、100、200IU/ml)重组改构人肿瘤坏死因子(rmhTNF)处理胃癌细胞MKN45,增殖/毒性检测试剂盒(CCK-8)观察其细胞增殖抑制率;实时荧光定量PCR(RT-PCR)法检测MKN45细胞p53异构体Δ133p53、STAT1及STAT3 m RNA的表达变化。[结果 ]CCK-8结果显示,随rmhTNF作用浓度增高(50、100、200IU/ml),MKN45细胞抑制率分别为17.133%,24.800%和31.733%,差异有统计学意义(F=16.246,P〈0.01)。RT-PCR结果显示,随rmhTNF浓度增高,MKN45细胞STAT1 m RNA表达上升(F=164.290,P〈0.001),STAT3、Δ133p53 m RNA表达下降(F=29.921,F=24.243;P均〈0.001)。Pearson相关性分析结果显示,Δ133p53与STAT1表达呈负相关(r=-0.951,P〈0.01),与STAT3表达呈正相关(r=0.840,P〈0.01)。[结论 ]MKN45细胞中,Δ133p53是STAT1、STAT3调控肿瘤细胞的共同靶基因,STAT1、STAT3-Δ133p53-p53通路可能是rmhTNF抑制胃癌细胞MKN45的机制。[Objective] To investigate the biological effects and mechanisms of rmhTNF on gastric cancer cell line MKN45.[Methods] The different concentrations(50,100,200 IU/ml) of recombined and modified human tumor necrosis factor(rmhTNF) were used in gastric carcinoma cell line MKN45.The growth inhibition rate of rmhTNF was observed by CCK8 assay. The mRNA expressions of p53 is forms Δ133 p53,STAT1,and STAT3 on MKN45 gastric cancer cells were detected by realtime polymerase chain reaction(RT-PCR).[Results] CCK-8 assay showed that as rmhTNF concentrations(50,100,200 IU/ml) increased,the inhibitory rates of MKN45 cells increased accordingly(17.133%,24.800%,and 31.733%,respectively),and that the difference was statistically significant(F =16.246,P〈0.01). RT-PCR showed that as rmhTNF concentrations increased,the expression of STAT1 mRNA in MKN45 cells also increased(F=164.290,P〈0.01)while the expression of STAT3,delta 133 p53 mRNA decreased(F=29.921,F=24.243,all P〈0.01). Pearson correlation analysis showed that the expression of delta 133 p53 was negatively correlated with that of STAT1 and positively correlated with that of STAT3(r =-0.951,r =0.840,all P〈0.01). [Conclusion] In MKN45,Δ133 p53 is the common target gene of both STAT1 and STAT3 in regulating tumor cells,and STAT1,STAT3-Δ133 p53-p53 pathway may be the mechanism of rmhTNF inhibiting gastric cancer cell line MKN45.
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