| 袁明亮,季万胜,初国艳.rmhTNF联合顺铂抑制人胃癌细胞增殖的作用机制[J].中国肿瘤,2015,24(8):702-707. |
| rmhTNF联合顺铂抑制人胃癌细胞增殖的作用机制 |
| The Mechanism of rmhTNF Combined with Cisplatin Inhibit the Proliferation of Human Gastric Cancer Cells |
| 投稿时间：2014-12-19 |
| DOI：10.11735/j.issn.1004-0242.2015.08.A015 |
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| 中文关键词: rmhTNF 顺铂 胃癌 p53β caspase-3 |
| 英文关键词:rmhTNF 顺铂 胃癌 p53β caspase-3 |
| 基金项目:山东省优秀中青年科学家科研奖励基金（BS2010SW034） |
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| 中文摘要: |
| 摘 要：［目的］探讨rmhTNF联合顺铂抑制人胃癌细胞增殖的作用机制。［方法］不同浓度rmhTNF（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 mRNA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rmhTNF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rmhTNF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rmhTNF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 mRNA表达均增加，且联合组均高于单独组并随rmhTNF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rmhTNF组中未见明显改变，差异无统计学意义（F=0.006，P>0.05），rmhTNF联合顺铂作用时可明显上调p53β的表达，并且随rmhTNF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 mRNA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］ rmhTNF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。 |
| 英文摘要: |
| Abstract：［Purpose］ To investigate the mechanism of rmhTNF combined with cisplatin inhibit the proliferation of human gastric cancer cells. ［Methods］ Different concentrations rmhTNF (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-3 mRNA expression in MKN45 and SGC7901 were determined by Nested reverse transcription polymerase chain reaction (nRT-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 rmhTNF concentration increased，the difference was statistically significant，but there is no such phenomenon in SGC7901 gastric cancer cells and when different concentrations of rmhTNF 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 rmhTNF monotherapy groups with the increase of rmhTNF 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 monotherapy groups and with the increase of rmhTNF concentration increased，the difference was statistically significant (F=93.889，P<0.05)；p53β has no significant change in monotherapy groups of rmhTNF，the difference was not statistically significant（F=0.006，P>0.05）.Combined intervention can significantly up regulated p53β and p53β increases with rmhTNF concentration，the difference was statistically significant（F=18.577，P<0.001）. In SGC7901 gastric cancer cells the expression of p53β mRNA was not observed，the trend expression of caspase-3 mRNA was same with MKN45，the difference was statistically significant （F=1409.656，P<0.005）. Person correlation analysis showed that，the expression of p53β and caspase-3 was positively correlated（r=0.766，P<0.001），inhibition rate was positively correlated with the expression of caspase-3 (r=0.978，P<0.001). ［Conclusion］ The synergistic inhibitory mechanisms about rmhTNF combined with cisplatin on gastric cancer cell line MKN45 may through activating p53β to up regulate caspase-3. |
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