Cancer-derived VEGF plays no role in malignant ascites formation in the mouse

被引:8
作者
Guleng, Bayasi [1 ]
Tateishi, Keisuke [1 ]
Kanai, Fumihiko [1 ,2 ]
Jazag, Amarsanaa [1 ]
Ohta, Miki [1 ]
Asaoka, Yoshinari [1 ]
Ijichi, Hideaki [1 ]
Tanaka, Yasuo [1 ]
Imamura, Jun [1 ]
Ikenoue, Tsuneo [1 ]
Fukushima, Yasushi [1 ]
Morikane, Keita [3 ]
Miyagishi, Makoto [4 ]
Taira, Kazunari [4 ]
Kawabe, Takao [1 ]
Omata, Masao [1 ,2 ]
机构
[1] Univ Tokyo, Dept Gastroenterol, Grad Sch Med, Bunkyo Ku, Tokyo 1138655, Japan
[2] Univ Tokyo Hosp, Clin Res Ctr, Bunkyo Ku, Tokyo 1138655, Japan
[3] Natl Inst Infect Dis, Infect Dis Surveillance Ctr, Shinjuku Ku, Tokyo 1628640, Japan
[4] Univ Tokyo, Grad Sch Engn, Dept Chem & Biotechnol, Tokyo 1138656, Japan
关键词
VEGF; Ascites; RNAi;
D O I
10.3748/wjg.v11.i35.5455
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
AIM: Vascular endothelial growth factor (VEGF) is a potent mediator of peritoneal fluid accumulation following tumor progression. This study investigated the role of VEGF secreted by cancerous cells in the formation of malignant ascites. METHODS: VEGF expression was eliminated by knockdown in the pancreas cancer cell-line PancO2 using vector-based short-hairpin type RNA interference (RNAi). Malignant ascites formation in the mouse was analyzed by intraperitoneal injection of PancO2 cells expressing VEGF or with expression knockdown. RESULTS: The VEGF knockdown PancO2 cell was successfully established. Knockdown of VEGF did not affect cancer cell proliferation in vitro or in vivo. The volume of ascites following peritoneal expansion of the tumor in VEGF knockdown cells and control cells did not differ statistically in this in vivo study. Moreover, the VEGF concentration in the ascites did not differ statistically. CONCLUSION: Malignant ascites formation might be mediated by VEGF production in noncancerous tissues, such as stromal compartments. An anti-VEGF strategy against malignant ascites could be applied to various tumors regardless of whether they secrete VEGF. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.
引用
收藏
页码:5455 / 5459
页数:5
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