四川大学学报(医学版)
四川大學學報(醫學版)
사천대학학보(의학판)
JOURNAL OF WEST CHINA UNIVERSITY OF MEDICAL SCIENCES
2010年
1期
10-14,28
,共6页
芮军%龙丹%王伟%仇滔%张志国%黎新建%方冰%袁武%罗勇%周静
芮軍%龍丹%王偉%仇滔%張誌國%黎新建%方冰%袁武%囉勇%週靜
예군%룡단%왕위%구도%장지국%려신건%방빙%원무%라용%주정
丙戊酸钠%肺癌细胞%MHCⅠ类链相关基因A%NK细胞
丙戊痠鈉%肺癌細胞%MHCⅠ類鏈相關基因A%NK細胞
병무산납%폐암세포%MHCⅠ류련상관기인A%NK세포
Valproic acid%Lung carcinoma cell%MICA%NK cells
目的 观察丙戊酸钠(valproic acid,VPA)对人肺癌细胞A549、SP-CA-1、NCIH446中的MHCⅠ类链相关基因A(MICA)表达的影响,并比较肺癌细胞经VPA处理前后NK细胞对其杀伤作用的差异.方法 将0.75～12.0 mmol/L VPA作用于A549、SP-CA-1、NCIH446细胞,与未加VPA的对照组进行比较,观察VPA对人肺癌细胞生长的影响.选择对细胞生长无影响的1.50 mmol/L和3.00 mmol/L VPA诱导3株肺癌细胞4 d,通过RT-PCR反应和免疫荧光法分别检测MICA在mRNA和蛋白质水平的变化.LDH法检测VPA处理肺癌细胞前后其被NK细胞杀伤程度的变化.结果 ＞6.0 mmol/L VPA对3株肺癌细胞均表现出抑制其生长.用1.50mmol/L和3.00 mmol/L VPA诱导4 d后的3株肺癌细胞,与对照组比较,其MICA的mRNA转录水平和蛋白质表达提高(P＜0.05);1.50 mmol/L和3.00 mmol/L VPA诱导表达MICA后的肺癌细胞均比未经VPA处理的肺癌细胞被NK杀伤的程度高(P＜0.05).3.00 mmol/L VPA浓度组3株肺癌细胞的MICA mRNA、蛋白质表达水平及其被NK细胞杀伤的程度均高于1.50 mmol/L VPA浓度组(P＜0.05).结论 VPA通过上调MICA抗肺癌作用的新机制,为肺癌临床免疫生物治疗提供了实验依据.
目的 觀察丙戊痠鈉(valproic acid,VPA)對人肺癌細胞A549、SP-CA-1、NCIH446中的MHCⅠ類鏈相關基因A(MICA)錶達的影響,併比較肺癌細胞經VPA處理前後NK細胞對其殺傷作用的差異.方法 將0.75～12.0 mmol/L VPA作用于A549、SP-CA-1、NCIH446細胞,與未加VPA的對照組進行比較,觀察VPA對人肺癌細胞生長的影響.選擇對細胞生長無影響的1.50 mmol/L和3.00 mmol/L VPA誘導3株肺癌細胞4 d,通過RT-PCR反應和免疫熒光法分彆檢測MICA在mRNA和蛋白質水平的變化.LDH法檢測VPA處理肺癌細胞前後其被NK細胞殺傷程度的變化.結果 ＞6.0 mmol/L VPA對3株肺癌細胞均錶現齣抑製其生長.用1.50mmol/L和3.00 mmol/L VPA誘導4 d後的3株肺癌細胞,與對照組比較,其MICA的mRNA轉錄水平和蛋白質錶達提高(P＜0.05);1.50 mmol/L和3.00 mmol/L VPA誘導錶達MICA後的肺癌細胞均比未經VPA處理的肺癌細胞被NK殺傷的程度高(P＜0.05).3.00 mmol/L VPA濃度組3株肺癌細胞的MICA mRNA、蛋白質錶達水平及其被NK細胞殺傷的程度均高于1.50 mmol/L VPA濃度組(P＜0.05).結論 VPA通過上調MICA抗肺癌作用的新機製,為肺癌臨床免疫生物治療提供瞭實驗依據.
목적 관찰병무산납(valproic acid,VPA)대인폐암세포A549、SP-CA-1、NCIH446중적MHCⅠ류련상관기인A(MICA)표체적영향,병비교폐암세포경VPA처리전후NK세포대기살상작용적차이.방법 장0.75～12.0 mmol/L VPA작용우A549、SP-CA-1、NCIH446세포,여미가VPA적대조조진행비교,관찰VPA대인폐암세포생장적영향.선택대세포생장무영향적1.50 mmol/L화3.00 mmol/L VPA유도3주폐암세포4 d,통과RT-PCR반응화면역형광법분별검측MICA재mRNA화단백질수평적변화.LDH법검측VPA처리폐암세포전후기피NK세포살상정도적변화.결과 ＞6.0 mmol/L VPA대3주폐암세포균표현출억제기생장.용1.50mmol/L화3.00 mmol/L VPA유도4 d후적3주폐암세포,여대조조비교,기MICA적mRNA전록수평화단백질표체제고(P＜0.05);1.50 mmol/L화3.00 mmol/L VPA유도표체MICA후적폐암세포균비미경VPA처리적폐암세포피NK살상적정도고(P＜0.05).3.00 mmol/L VPA농도조3주폐암세포적MICA mRNA、단백질표체수평급기피NK세포살상적정도균고우1.50 mmol/L VPA농도조(P＜0.05).결론 VPA통과상조MICA항폐암작용적신궤제,위폐암림상면역생물치료제공료실험의거.
Objective To investigate the effect of valproic acid(VPA)on MICA gene expression in human lung carcinoma cell lines:A549,SP-CA-1,NCIH446.Methods Different concentration of VPA were applied to treat A549,SP-CA-1,NCIH446 cells respectively and the untreated cells as the control.The effect of the VPA on the cells were observed.Reverse Transcriptase PCR and Immune-Fluorescence staining were used to detect the changes of mRNA.protein level of MICA gene in the three cell lines treated with 1.50 mmol/L and 3.00 mmol/L VPA for 4 days.under the concentration of VPA from 0.75 to 12.0 mmol/L.The viability of lung cancer cells after NK effect in the VPA(+)and VPA(-)treatment were evaluated with LDH method.Results The inhibition effects were observed when the VPA concentration was 6.0 mmol/L above compared to control group,VPA induced the increasing expression of MICA and in turn enhanced the NK killing effect on the cells in a concentrationdepended pattern.Conclusion VPA induced MICA expression,NK killing effect in the VPA(+)treatment lung cancer cells was significantly stronger than that of VPA(-)condition,which implied a new mechanism of anticancer method and could be a new approach to cancer therapy.
