Lee Sang Y, Slagle-Webb Becky, Rizk Elias, Patel Akshal, Miller Patti A, Sung Shen-Shu, Connor James R
Department of Neurosurgery, Pennsylvania State University College of Medicine, Penn State M.S. Hershey Medical Center, Hershey, Pennsylvania, United States of America.
Department of Radiology, Pennsylvania State University College of Medicine, Penn State M.S. Hershey Medical Center, Hershey, Pennsylvania, United States of America.
PLoS One. 2014 Sep 25;9(9):e108166. doi: 10.1371/journal.pone.0108166. eCollection 2014.
The standard chemotherapy for brain tumors is temozolomide (TMZ), however, as many as 50% of brain tumors are reportedly TMZ resistant leaving patients without a chemotherapeutic option. We performed serial screening of TMZ resistant astrocytoma cell lines, and identified compounds that are cytotoxic to these cells. The most cytotoxic compound was an analog of thiobarbituric acid that we refer to as CC-I. There is a dose-dependent cytotoxic effect of CC-I in TMZ resistant astrocytoma cells. Cell death appears to occur via apoptosis. Following CC-I exposure, there was an increase in astrocytoma cells in the S and G2/M phases. In in vivo athymic (nu/nu) nude mice subcutaneous and intracranial tumor models, CC-I completely inhibited tumor growth without liver or kidney toxicity. Molecular modeling and enzyme activity assays indicate that CC-I selectively inhibits topoisomerase IIα similar to other drugs in its class, but its cytotoxic effects on astrocytoma cells are stronger than these compounds. The cytotoxic effect of CC-I is stronger in cells expressing unmethylated O6-methylguanine methyltransferase (MGMT) but is still toxic to cells with methylated MGMT. CC-I can also enhance the toxic effect of TMZ on astrocytoma when the two compounds are combined. In conclusion, we have identified a compound that is effective against astrocytomas including TMZ resistant astrocytomas in both cell culture and in vivo brain tumor models. The enhanced cytotoxicity of CC-I and the safety profile of this family of drugs could provide an interesting tool for broader evaluation against brain tumors.
脑肿瘤的标准化疗药物是替莫唑胺(TMZ),然而,据报道多达50%的脑肿瘤对TMZ耐药,导致患者没有化疗选择。我们对TMZ耐药的星形细胞瘤细胞系进行了系列筛选,并鉴定出对这些细胞具有细胞毒性的化合物。细胞毒性最强的化合物是硫代巴比妥酸类似物,我们将其称为CC-I。CC-I对TMZ耐药的星形细胞瘤细胞具有剂量依赖性的细胞毒性作用。细胞死亡似乎是通过凋亡发生的。暴露于CC-I后,处于S期和G2/M期的星形细胞瘤细胞数量增加。在体内无胸腺(nu/nu)裸鼠皮下和颅内肿瘤模型中,CC-I完全抑制肿瘤生长,且无肝或肾毒性。分子建模和酶活性测定表明,CC-I与该类中的其他药物类似,选择性抑制拓扑异构酶IIα,但其对星形细胞瘤细胞的细胞毒性作用比这些化合物更强。CC-I对表达未甲基化O6-甲基鸟嘌呤甲基转移酶(MGMT)的细胞的细胞毒性作用更强,但对甲基化MGMT的细胞仍有毒性。当这两种化合物联合使用时,CC-I还可以增强TMZ对星形细胞瘤的毒性作用。总之,我们已经鉴定出一种在细胞培养和体内脑肿瘤模型中对星形细胞瘤(包括TMZ耐药的星形细胞瘤)有效的化合物。CC-I增强的细胞毒性和该类药物的安全性可能为更广泛地评估针对脑肿瘤的治疗提供一个有趣的工具。