Akutagawa Noriyuki, Nishikawa Akira, Iwasaki Masahiro, Fujimoto Takashi, Teramoto Mizue, Kitajima Yoshimitsu, Endo Toshiaki, Shibuya Masabumi, Kudo Ryuichi
Department of Obstetrics and Gynecology, School of Medicine, Sapporo Medical University, Chuo-ku, Sapporo 060-8543.
Jpn J Cancer Res. 2002 Jun;93(6):644-51. doi: 10.1111/j.1349-7006.2002.tb01302.x.
Ascites formation and peritoneal dissemination are critical problems in patients with advanced ovarian cancer. Vascular endothelial growth factor (VEGF), also known as angiogenic growth factor, is a potent mediator of peritoneal fluid accumulation and angiogenesis of tumors. E-Cadherin is an adhesion molecule that is important for cell-to-cell interaction. To elucidate the molecular mechanism of ascites formation and peritoneal dissemination of ovarian cancer, we examined the expression of VEGF and E-cadherin in different ovarian cancer cell lines and utilized nude mice to compare the biological characteristics of ovarian cancer cells. Three human ovarian cancer cell lines (AMOC-2, HNOA and HTBOA) were used in this study. Expression of genes was analyzed by northern blotting and RT-PCR methods. AMOC-2 expressed E-cadherin, but not VEGF. HNOA expressed VEGF without E-cadherin expression. HTBOA expressed both VEGF and E-cadherin. Each human ovarian cancer model revealed a specific feature. The AMOC-2 mouse had a single large peritoneal tumor without ascites or remarkable peritoneal dissemination. HTBOA and HNOA mice had bloody ascites and marked peritoneal dissemination. Introduction of VEGF antisense into HTBOA cells could inhibit the ascites formation. It is suggested that VEGF is important for the ascites formation via the increased vascular permeability effect. The deregulation of E-cadherin expression might be involved in the peritoneal dissemination. These molecules are important for the formation of specific features of advanced ovarian cancer. Ovarian cancer cell lines that had different gene expression patterns produced nude mouse human ovarian cancer models with different characteristics.
腹水形成和腹膜播散是晚期卵巢癌患者面临的关键问题。血管内皮生长因子(VEGF),也被称为血管生成生长因子,是腹膜液积聚和肿瘤血管生成的强效介质。E-钙黏蛋白是一种对细胞间相互作用很重要的黏附分子。为了阐明卵巢癌腹水形成和腹膜播散的分子机制,我们检测了不同卵巢癌细胞系中VEGF和E-钙黏蛋白的表达,并利用裸鼠比较卵巢癌细胞的生物学特性。本研究使用了三种人卵巢癌细胞系(AMOC-2、HNOA和HTBOA)。通过Northern印迹法和RT-PCR方法分析基因表达。AMOC-2表达E-钙黏蛋白,但不表达VEGF。HNOA表达VEGF但不表达E-钙黏蛋白。HTBOA同时表达VEGF和E-钙黏蛋白。每种人卵巢癌模型都显示出特定特征。AMOC-2小鼠有一个单一的大腹膜肿瘤,没有腹水或明显的腹膜播散。HTBOA和HNOA小鼠有血性腹水和明显的腹膜播散。将VEGF反义核酸导入HTBOA细胞可抑制腹水形成。提示VEGF通过增加血管通透性作用对腹水形成很重要。E-钙黏蛋白表达失调可能与腹膜播散有关。这些分子对晚期卵巢癌特定特征的形成很重要。具有不同基因表达模式的卵巢癌细胞系产生了具有不同特征的裸鼠人卵巢癌模型。