Lindsay C K, Gomez D E, Thorgeirsson U P
Tumor Biology and Carcinogenesis Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Anticancer Res. 1996 Jan-Feb;16(1):425-31.
Flavone acetic acid (FAA) causes regression of a range of slow growing solid tumors implanted subcutaneously in mice. Although its precise mechanism of action is unknown, vascular collapse has been shown to precede tumor growth delay and regression. The aim of this study was to determine whether or not endothelial cell function was directly affected by clinically relevant concentrations of FAA. FAA at 100-250 micrograms/ml inhibited endothelial cell proliferation in vitro, but did not compromise cellular function or viability. FAA abolished tubule formation in an in vitro angiogenesis assay and reduced vascular development of the chick embryo chorioallantoic membrane. In addition to targeting established tumor vasculature, FAA may also affect proliferating endothelium which may be involved in mediating the reduced tumor growth rate or stasis often often observed after drug exposure. The chorioallantoic membrane of the chick embryo may represent an important model to elucidate more clearly the effect of FAA on a growing vascular network.
黄酮醋酸（FAA）可使小鼠皮下植入的多种生长缓慢的实体瘤消退。尽管其确切作用机制尚不清楚，但已表明血管塌陷先于肿瘤生长延迟和消退。本研究的目的是确定临床相关浓度的FAA是否直接影响内皮细胞功能。100 - 250微克/毫升的FAA在体外抑制内皮细胞增殖，但不损害细胞功能或活力。FAA在体外血管生成试验中消除了小管形成，并减少了鸡胚绒毛尿囊膜的血管发育。除了靶向已建立的肿瘤血管系统外，FAA还可能影响增殖的内皮细胞，这可能参与介导药物暴露后经常观察到的肿瘤生长速率降低或停滞。鸡胚绒毛尿囊膜可能是一个重要的模型，可更清楚地阐明FAA对生长中的血管网络的影响。
