中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2010年
10期
1297-1300
,共4页
丁兆军%孟令新%李江涛%孙树艳%陈希平%雷铭德
丁兆軍%孟令新%李江濤%孫樹豔%陳希平%雷銘德
정조군%맹령신%리강도%손수염%진희평%뢰명덕
神经生长因子类/投药和剂量%受体,神经生长因子类/投药和剂量%胰腺肿瘤/药物疗法%肿瘤侵润%肿瘤转移
神經生長因子類/投藥和劑量%受體,神經生長因子類/投藥和劑量%胰腺腫瘤/藥物療法%腫瘤侵潤%腫瘤轉移
신경생장인자류/투약화제량%수체,신경생장인자류/투약화제량%이선종류/약물요법%종류침윤%종류전이
Nerve growth factors/AD%Receptors,nerve growth factor /AD%Pancreatic neoplasms/DT%Neoplasm invasiveness%Neoplasm metastasis
目的 探讨Artemin及其受体GFRα3对MIA PaCa-2人胰腺癌细胞浸润转移能力的影响.方法 以MIA PaCa-2人胰腺癌细胞为研究对象,采用Transwell Chamber分析不同浓度的Artemin及受体GFRα3对胰腺癌细胞浸润转移能力的影响,MIA PaCa-2胰腺癌细胞经Artemin及受体GFRα3刺激后,采用RT-PCR及Western blot方法定量分析MIA PaCa-2细胞中基质金属蛋白酶-2(MMP-2)、上皮钙粘附素(E-cadherin)表达水平的变化.结果 随着Artemin及受体GFRα3作用浓度的增加,MIA PaCa-2胰腺癌细胞浸润转移能力明显增强,均明显高于对照组[150 ng/ml浓度:Artemin组:107.4±11.4;GFRα3组:94.4±9.3;对照组:34.6±7.3,P<0.01].150 ng/ml为二者的最佳作用浓度.经150 ng/ml Artemin、GFRα3分别作用后,MIA PaCa-2细胞合成MMP-2明显增加[Artemin组:(2.17±0.05)×108;GFRα3组:(2.02±0.03)×108;对照组:(1.02±0.02)×108,t=6.35,7.32],而E-cadherin明显降低[Artemin组:(0.65±0.04)×108;GFRα3组:(0.74±0.01)×108;对照组:(1.36±0.03)×108,t=4.27,5.61],与对照组比较差异均有统计学意义(P<0.01).结论 Artemin及其受体GFRα3可促进胰腺癌细胞的浸润和转移能力,可能与浸润转移相关分子MMP-2表达上调、E-cadherin表达下调有关.
目的 探討Artemin及其受體GFRα3對MIA PaCa-2人胰腺癌細胞浸潤轉移能力的影響.方法 以MIA PaCa-2人胰腺癌細胞為研究對象,採用Transwell Chamber分析不同濃度的Artemin及受體GFRα3對胰腺癌細胞浸潤轉移能力的影響,MIA PaCa-2胰腺癌細胞經Artemin及受體GFRα3刺激後,採用RT-PCR及Western blot方法定量分析MIA PaCa-2細胞中基質金屬蛋白酶-2(MMP-2)、上皮鈣粘附素(E-cadherin)錶達水平的變化.結果 隨著Artemin及受體GFRα3作用濃度的增加,MIA PaCa-2胰腺癌細胞浸潤轉移能力明顯增彊,均明顯高于對照組[150 ng/ml濃度:Artemin組:107.4±11.4;GFRα3組:94.4±9.3;對照組:34.6±7.3,P<0.01].150 ng/ml為二者的最佳作用濃度.經150 ng/ml Artemin、GFRα3分彆作用後,MIA PaCa-2細胞閤成MMP-2明顯增加[Artemin組:(2.17±0.05)×108;GFRα3組:(2.02±0.03)×108;對照組:(1.02±0.02)×108,t=6.35,7.32],而E-cadherin明顯降低[Artemin組:(0.65±0.04)×108;GFRα3組:(0.74±0.01)×108;對照組:(1.36±0.03)×108,t=4.27,5.61],與對照組比較差異均有統計學意義(P<0.01).結論 Artemin及其受體GFRα3可促進胰腺癌細胞的浸潤和轉移能力,可能與浸潤轉移相關分子MMP-2錶達上調、E-cadherin錶達下調有關.
목적 탐토Artemin급기수체GFRα3대MIA PaCa-2인이선암세포침윤전이능력적영향.방법 이MIA PaCa-2인이선암세포위연구대상,채용Transwell Chamber분석불동농도적Artemin급수체GFRα3대이선암세포침윤전이능력적영향,MIA PaCa-2이선암세포경Artemin급수체GFRα3자격후,채용RT-PCR급Western blot방법정량분석MIA PaCa-2세포중기질금속단백매-2(MMP-2)、상피개점부소(E-cadherin)표체수평적변화.결과 수착Artemin급수체GFRα3작용농도적증가,MIA PaCa-2이선암세포침윤전이능력명현증강,균명현고우대조조[150 ng/ml농도:Artemin조:107.4±11.4;GFRα3조:94.4±9.3;대조조:34.6±7.3,P<0.01].150 ng/ml위이자적최가작용농도.경150 ng/ml Artemin、GFRα3분별작용후,MIA PaCa-2세포합성MMP-2명현증가[Artemin조:(2.17±0.05)×108;GFRα3조:(2.02±0.03)×108;대조조:(1.02±0.02)×108,t=6.35,7.32],이E-cadherin명현강저[Artemin조:(0.65±0.04)×108;GFRα3조:(0.74±0.01)×108;대조조:(1.36±0.03)×108,t=4.27,5.61],여대조조비교차이균유통계학의의(P<0.01).결론 Artemin급기수체GFRα3가촉진이선암세포적침윤화전이능력,가능여침윤전이상관분자MMP-2표체상조、E-cadherin표체하조유관.
Objective To investigate the effects of artemin and its receptor GFRα - 3 on the invasion and metastasis of pancreatic cancer cells. Methods Human pancreatic cancer cell line MIA PaCa -2 was used in this study. Transwell cell culture chamber assay in vitro was used to detect the ability of invasion and metastasis of MIA PaCa -2 cells. The influence of artemin and GFRα -3 on the protein expression of MMP-2 and E-cadherin was investigated by Western blot and quantitative real time polymerase chain reaction-analyses (Q-RT-PCR). Results As the increase of artemin and GFRα -3, the invasion and metastasis of MIA PaCa- 2 was markedly increased [ 150 ng / ml concentration: Artemin group: 107.4 ± 11.4;GFRα3 group:94. 4 ± 9. 3 ;control group:34. 6 ± 7. 3, P < 0. 01 ]. With 150 ng / ml artemin and GFR-3,the synthesis of MMP-2 in MIA PaCa 2 cells was significantly increased than that in control group[ Artemin grou: (2. 17 ± 0. 05 ) × 108; GFRα3 group: (2. 02 ± 0. 03 ) × 108; control group: ( 1.02 ± 0. 02 ) × 108, t =6. 35,7. 32 ], while E-cadherin significantly decreased [ Artemin group: ( 0. 65 ± 0. 04 ) × 108; GFRα3 group: (0. 74 ± 0. 01 ) × 108; control group: ( 1. 36 ± 0. 03 ) × 108, t = 4. 27,5.61 ], the difference was statistically significant ( P <0. 01 ). Conclusions Artemin and its receptor GFRα3 could promote pancreatic cancer cell invasion and metastasis. This effect may be related to the up-regulated expression of MMP-2 and down regulated expression of E-cadherin.