MSX2 overexpression inhibits gemcitabine-induced caspase-3 activity in pancreatic cancer cells

被引：4

作者：

Hamada, Shin ^{[1
]}

Satoh, Kennichi ^{[1
]}

Kimura, Kenji ^{[1
]}

Kanno, Atsushi ^{[1
]}

Masamune, Atsushi ^{[1
]}

Shimosegawa, Tooru ^{[1
]}

机构：

[1] Tohoku Univ, Grad Sch Med, Div Gastroenterol, Aoba Ku, Sendai, Miyagi 9808574, Japan

来源：

WORLD JOURNAL OF GASTROENTEROLOGY | 2005年 / 11卷 / 43期

关键词：

MSX2; Caspase-3; Gemcitabine;

D O I：

10.3748/wjg.v11.i43.6867

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

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. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.

引用

页码：6867 / 6870

页数：4

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