MSX2 overexpression inhibits gemcitabine-induced caspase-3 activity in pancreatic cancer cells.
MSX2 overexpression inhibits gemcitabine-induced caspase-3 activity in pancreatic cancer cells.
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DOI：
10.3748/wjg.v11.i43.6867
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发表时间：
2005-11
影响因子：
4.3
通讯作者：
S. Hamada;K. Satoh;K. Kimura;A. Kanno;A. Masamune;T. Shimosegawa
中科院分区：
文献类型：
--
作者：
S. Hamada;K. Satoh;K. Kimura;A. Kanno;A. Masamune;T. Shimosegawa
目的探讨MSX2对吉西他滨诱导胰腺癌细胞株PANC-1中caspase-3活化的影响。方法利用V5标记的MSX2表达载体，从PANC-1细胞(Px14细胞)获得稳定的MSX2表达载体。用四甲基偶氮唑盐比色法测定吉西他滨作用下的细胞存活率，对照细胞系(空载体转染的PANC-1细胞；P-3EV细胞)。Hoechst染色检测细胞凋亡。用Western blotting分析和直接测定caspase-3的特异性活性来评价caspase-3的活性。结果在PANC-1细胞中过表达MSX2可降低吉西他滨诱导的caspase-3活性，增加吉西他滨作用下Px14细胞的存活率。结论MSX2对吉西他滨诱导的细胞凋亡途径具有抑制作用。MSX2这种新的细胞凋亡调节功能可能为胰腺癌的治疗提供新的靶点。
AIM To evaluate the effect of MSX2 on gemcitabine-induced caspase-3 activation in pancreatic cancer cell line Panc-1. METHODS Using V5-tagged MSX2 expression vector, stable transfectant of MSX2 was generated from Panc-1 cells (Px14 cells). Cell viability under gemcitabine administration was determined by MTT assay relative to control cell line (empty-vector transfected Panc-1 cells; P-3EV cells). Hoechst staining was used for the detection of apoptotic cell. Activation of caspase-3 was assessed using Western blotting analysis and direct measurement of caspase-3 specific activities. RESULTS MSX2 overexpression in Panc-1 cells resulted in decreased gemcitabine-induced caspase-3 activation and increased cell viability under gemcitabine treatment in Px14 cells. CONCLUSION MSX2 exerts repressive effects on gemcitabine-induced apoptotic pathway. This novel apoptosis-regulating function of MSX2 may provide a new therapeutic target for pancreatic cancer.