Kurebayashi J, Otsuki T, Kurosumi M, Soga S, Akinaga S, Sonoo H
Department of Breast & Thyroid Surgery, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
Jpn J Cancer Res. 2001 Dec;92(12):1342-51. doi: 10.1111/j.1349-7006.2001.tb02159.x.
A novel oxime derivative of radicicol, KF58333, binds to the heat shock protein 90 (Hsp90) and destabilizes its associated signaling molecules. These effects play a critical role in the growth inhibition of tumor cells. To further investigate the effects of this agent, it was administered to two human breast cancer cell lines, KPL-1 and KPL-4, both in vitro and in vivo. KF58333 dose-dependently inhibited the growth and vascular endothelial growth factor (VEGF) secretion, concomitantly with a decrease in VEGF mRNA expression, in each cell line. This agent also suppressed the increase of VEGF secretion and expression induced by hypoxia (1% O(2)). Intravenous injections of this agent into nude mice bearing either KPL-1 or KPL-4 xenografts significantly inhibited the tumor growth associated with a decrease in the Ki67 labeling index and microvascular area and an increase in apoptosis and the necrotic area. These findings indicate that the antitumor activity of this radicicol derivative may be partly mediated by decreasing VEGF secretion from tumor cells and inhibiting tumor angiogenesis. To explore the action mechanisms of the anti-angiogenic effect, the expression level of hypoxia-inducible factor (HIF)-1alpha was investigated. KF58333 provided a significant decrease in the HIF-1alpha protein expression under both normoxic and hypoxic conditions. In contrast, the mRNA expression of HIF-1alpha was not decreased by this agent. It is suggested that the post-transcriptional down-regulation of HIF-1alpha expression by this agent may result in a decrease of VEGF expression and tumor angiogenesis.
一种新型的萝卜硫素肟衍生物KF58333,可与热休克蛋白90(Hsp90)结合并使其相关信号分子不稳定。这些作用在肿瘤细胞的生长抑制中起关键作用。为进一步研究该药物的作用,对两种人乳腺癌细胞系KPL-1和KPL-4进行了体内外实验。KF58333在每个细胞系中均呈剂量依赖性地抑制生长和血管内皮生长因子(VEGF)分泌,同时VEGF mRNA表达降低。该药物还抑制了缺氧(1% O₂)诱导的VEGF分泌和表达增加。将该药物静脉注射到携带KPL-1或KPL-4异种移植瘤的裸鼠体内,可显著抑制肿瘤生长,同时Ki67标记指数和微血管面积降低,凋亡和坏死面积增加。这些发现表明,这种萝卜硫素衍生物的抗肿瘤活性可能部分是通过减少肿瘤细胞VEGF分泌和抑制肿瘤血管生成来介导的。为探究抗血管生成作用的机制,研究了缺氧诱导因子(HIF)-1α的表达水平。在常氧和缺氧条件下,KF58333均可使HIF-1α蛋白表达显著降低。相比之下,该药物并未降低HIF-1α的mRNA表达。提示该药物对HIF-1α表达的转录后下调可能导致VEGF表达降低和肿瘤血管生成减少。