Guleng Bayasi, Tateishi Keisuke, Kanai Fumihiko, Jazag Amarsanaa, Ohta Miki, Asaoka Yoshinari, Ijichi Hideaki, Tanaka Yasuo, Imamura Jun, Ikenoue Tsuneo, Fukushima Yasushi, Morikane Keita, Miyagishi Makoto, Taira Kazunari, Kawabe Takao, Omata Masao
Department of Gastroenterology, Graduate School of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Tokyo 113-8655, Japan.
World J Gastroenterol. 2005 Sep 21;11(35):5455-9. doi: 10.3748/wjg.v11.i35.5455.
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.
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.
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.
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.
血管内皮生长因子（VEGF）是肿瘤进展后腹腔积液的强效介质。本研究调查了癌细胞分泌的VEGF在恶性腹水形成中的作用。
使用基于载体的短发夹型RNA干扰（RNAi）在胰腺癌细胞系PancO2中通过敲低消除VEGF表达。通过腹腔注射表达VEGF或表达敲低的PancO2细胞来分析小鼠恶性腹水的形成。
成功建立了VEGF敲低的PancO2细胞。VEGF敲低在体外或体内均不影响癌细胞增殖。在这项体内研究中，VEGF敲低细胞和对照细胞中肿瘤腹膜扩张后的腹水量在统计学上没有差异。此外，腹水中的VEGF浓度在统计学上也没有差异。
恶性腹水的形成可能由非癌组织（如基质区室）中的VEGF产生介导。针对恶性腹水的抗VEGF策略可应用于各种肿瘤，无论它们是否分泌VEGF。
