中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2010年
9期
1283-1285
,共3页
王磊%杨祖立%陈典克%宋顺心%兰平%汪建平
王磊%楊祖立%陳典剋%宋順心%蘭平%汪建平
왕뢰%양조립%진전극%송순심%란평%왕건평
胰腺癌%MKK4基因
胰腺癌%MKK4基因
이선암%MKK4기인
Pancreatic carcinoma%MKK4
目的 观察MKK4对胰腺癌细胞增生和浸润能力的影响.方法 采用Western blot检测常见胰腺癌细胞株中MKK4的表达;构建MKK4的腺病毒载体,感染不表达MKK4的胰腺癌细胞株,采用胸腺嘧啶标记法观察外源性MKK4表达对细胞增生能力的影响,采用体外细胞浸润实验观察外源性MKK4表达对细胞浸润能力的影响.结果 在胰腺癌细胞株AsPC1、BxPC3、Hs766T、MiapaCa2、Pancl中,MKK4在AsPC1和BxPC3细胞中表达缺失.成功构建MKK4的腺病毒载体.以腺病毒LacZ感染作对照,通过胸腺嘧啶标记法观察到AsPC1、BxPC3细胞感染MKK4腺病毒后,细胞增生能力增加53%、61%(P<0.05);通过体外细胞浸润实验观察到细胞浸润能力增强(8.2±2.7)倍、(15.7±1.6)倍(P<0.01).结论 MKK4在胰腺癌细胞中表达可增加其增生和浸润能力,具有潜在癌基因作用.
目的 觀察MKK4對胰腺癌細胞增生和浸潤能力的影響.方法 採用Western blot檢測常見胰腺癌細胞株中MKK4的錶達;構建MKK4的腺病毒載體,感染不錶達MKK4的胰腺癌細胞株,採用胸腺嘧啶標記法觀察外源性MKK4錶達對細胞增生能力的影響,採用體外細胞浸潤實驗觀察外源性MKK4錶達對細胞浸潤能力的影響.結果 在胰腺癌細胞株AsPC1、BxPC3、Hs766T、MiapaCa2、Pancl中,MKK4在AsPC1和BxPC3細胞中錶達缺失.成功構建MKK4的腺病毒載體.以腺病毒LacZ感染作對照,通過胸腺嘧啶標記法觀察到AsPC1、BxPC3細胞感染MKK4腺病毒後,細胞增生能力增加53%、61%(P<0.05);通過體外細胞浸潤實驗觀察到細胞浸潤能力增彊(8.2±2.7)倍、(15.7±1.6)倍(P<0.01).結論 MKK4在胰腺癌細胞中錶達可增加其增生和浸潤能力,具有潛在癌基因作用.
목적 관찰MKK4대이선암세포증생화침윤능력적영향.방법 채용Western blot검측상견이선암세포주중MKK4적표체;구건MKK4적선병독재체,감염불표체MKK4적이선암세포주,채용흉선밀정표기법관찰외원성MKK4표체대세포증생능력적영향,채용체외세포침윤실험관찰외원성MKK4표체대세포침윤능력적영향.결과 재이선암세포주AsPC1、BxPC3、Hs766T、MiapaCa2、Pancl중,MKK4재AsPC1화BxPC3세포중표체결실.성공구건MKK4적선병독재체.이선병독LacZ감염작대조,통과흉선밀정표기법관찰도AsPC1、BxPC3세포감염MKK4선병독후,세포증생능력증가53%、61%(P<0.05);통과체외세포침윤실험관찰도세포침윤능력증강(8.2±2.7)배、(15.7±1.6)배(P<0.01).결론 MKK4재이선암세포중표체가증가기증생화침윤능력,구유잠재암기인작용.
Objective To explore the effects of MKK4 gene on the proliferation and invasion of pancreatic cancer cells. Methods Western blotting was used to assay the expression of MKK4 in pancreatic cancer cell lines AsPC1, BxPC3, Hs766t, MiaPaCa2, and Pancl. MKK4 adenovirus was constructed and transfected into MKK4 negative pancreatic cancer cells. Thymidine incorporation assays were used to measure the DNA synthesis rate and Matrigel assays to measure the invasive ability of pancreatic cells. Results In pancreatic cancer cells, MKK4 lost expression in AsPC1 and BxPC3 cells. MKK4 adenovirus was constructed and transfected into MKK4 negative pancreatic cancer cell lines AsPC1 and BxPC3. The exogenous expression of MKK4 in AsPC1 and BxPC3 increased the proliferation ability by 53% and 61%( P < 0. 05 ), increased the invasion ability by ( 8. 2 ± 2. 7) fold and ( 15.7 ± 1.6) fold ( P < 0. 01 ), respectively. Conclusion The exogenous expression of MKK4 increases the proliferation and invasion of pancreatic cancer cells, which hints that MKK4 gene is a potential oncogene in pancreatic cancer.