Guleng B, Tateishi K, Kanai F, Jazag A, Ohta M, Asaoka Y, Ijichi H, Tanaka Y, Imamura J, Ikenoue T, Fukushima Y, Morikane K, Miyagishi M, Taira K, Kawabe T, Omata M. Cancer-derived VEGF plays no role in malignant ascites formation in the mouse. World J Gastroenterol 2005; 11(35): 5455-5459 [PMID: 16222736 DOI: 10.3748/wjg.v11.i35.5455]
Corresponding Author of This Article
Keisuke Tateishi, MD, PhD, Department of Gastroenterology, Graduate School of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. tateishik-int@h.u-tokyo.ac.jp
Article-Type of This Article
Basic Research
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Bayasi Guleng, Keisuke Tateishi, Fumihiko Kanai, Amarsanaa Jazag, Miki Ohta, Yoshinari Asaoka, Hideaki Ijichi, Yasuo Tanaka, Jun Imamura, Tsuneo Ikenoue, Yasushi Fukushima, Takao Kawabe, Masao Omata, Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
Fumihiko Kanai, Masao Omata, Clinical Research Center, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
Keita Morikane, Infectious Disease Surveillance Center, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan
Makoto Miyagishi, Kazunari Taira, Department of Chemistry and Biotechnology, Graduate School of Engineering, University of Tokyo, Tokyo 113-8656, Japan
Author contributions: All authors contributed equally to the work.
Correspondence to: Keisuke Tateishi, MD, PhD, Department of Gastroenterology, Graduate School of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. tateishik-int@h.u-tokyo.ac.jp
Telephone: +81-3-3815-5411 Fax: +81-3-3814-0021
Received: November 8, 2004 Revised: December 16, 2004 Accepted: December 20, 2004 Published online: September 21, 2005
Abstract
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.
