INHIBITION OF HEPATOCELLULAR CARCINOMA BY DEFEROXAMINE

人肝癌细胞株的抑制作用 评估并比较甲磺酸去铁胺（去铁胺）（DFX） 随着细胞在不存在DFX的情况下的生长以及随着 人肺成纤维细胞（WI 38）。 PLC/PRF/5或HepG 2维持7 在30（mu）M或60（mu）M DFX中的天数没有增加，到第7天， 产生很少或没有甲胎蛋白（AFP）。 无DFX的细胞生长 在第7天达到汇合，第7天AFP = 30-60 ng/ml (PLC/PRF/5）和> 1，000 ng/ml（HepG 2）。(Cell增长和 在3（mu）M DFX中的AFP产生轻度降低。B型肝炎滴度 PLC/PRF/5细胞产生的表面抗原（HBsAg）减少1-2 与无DFX生长的细胞相比，在30 AM和60（mu）M DFX中的对数。 用30 μ M或60 μ M DFX培养的WI-38细胞生长率为对照组的50%。 不含DFX的WI-38细胞。 DFX抑制PLC/PRF/5和HepG 2的生长 细胞以明显的剂量相关方式（30（mu）M或60（mu）M DFX 抑制细胞生长和AFP产生）相比， WI-38细胞率。 对PLC/PRF/5和HepG 2细胞的抑制作用可能与其对肝癌细胞的生长抑制有关。 部分是由于铁螯合作用以外的机制。 已经进行了许多额外的研究，以进一步评估这些 意见。 这些措施包括试图克服或防止 用不同的铁盐抑制，并评价抑制是否 在其他六种人肝癌细胞系中也以同样的方式发生。 的抑制 在所有人肝癌细胞中，去铁胺对肝癌细胞系的作用相似 测试的细胞系，无论来源国（南非， 美国、日本）或细胞中存在或不存在HBV DNA 线 在任何情况下，等摩尔浓度的铁（三价铁或 亚铁盐）阻止或逆转去铁胺的抑制作用。

Inhibition of several human hepatocellular carcinoma (HCC) cell lines by deferoxamine mesylate (desferrioxamine) (DFX) was evaluated and compared with growth of the cells in the absence of DFX and with the growth of human lung fibroblast (WI38) cells. PLC/PRF/5 or HepG2 maintained for 7 days in 30 (mu)M or 60 (mu)M DFX did not increase in number and by day 7 produced little or no alpha-fetoprotein (AFP). Cell growth without DFX reached confluence at day 7 and by day 7 had AFP = 30-60 ng/ml (PLC/PRF/5) and >1,000 ng/ml (HepG2) in the supernate. (Cell growth and AFP production in 3 (mu)M DFX were mildly reduced.) Titers of hepatitis B surface antigen (HBsAg) produced by the PLC/PRF/5 cells were reduced 1-2 logs in 30 AM and 60 (mu)M DFX compared to cells grown without DFX. WI-38 cells grown with 30 AM or 60 (mu)M DFX grew at 50% of the rate of WI-38 cells without DFX. DFX inhibits the growth of PLC/PRF/5 and HepG2 cells in an apparently dose-related manner (30 (mu)M or 60 (mu)M DFX arresting cell growth and AFP production) compared to reducing the growth rate of WI-38 cells. The inhibition of PLC/PRF/5 and HepG2 cells may be due, in part, to mechanisms other than iron chelation. Many additional studies have been conducted to further evaluate these observations. These have included attempts to overcome or prevent inhibition with different iron salts, and evaluating whether inhibition occurs in the same way in six other human HCC cell lines. The inhibition of HCC cell lines by deferoxamine occurred similarly in all human HCC cell lines tested, regardless of the country of origin (South Africa, United States, Japan) or the presence or absence of HBV DNA in the cell line. In no case could equimolar concentrations of iron (ferric or ferrous salts) prevent or reverse the inhibitory effect of deferoxamine.