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免疫调节药物来那度胺(Revlimid,通用名:lenalidomide)和CC - 4047通过激活自然杀伤细胞(NK细胞)诱导血液肿瘤细胞和实体瘤细胞凋亡。

Immunomodulatory drugs Revlimid (lenalidomide) and CC-4047 induce apoptosis of both hematological and solid tumor cells through NK cell activation.

作者信息

Zhu Dan, Corral Laura G, Fleming Yuedi W, Stein Bernd

机构信息

Celgene Corporation, 4550 Towne Centre Court, San Diego, CA, 92121, USA.

出版信息

Cancer Immunol Immunother. 2008 Dec;57(12):1849-59. doi: 10.1007/s00262-008-0512-7. Epub 2008 Apr 8.

Abstract

Revlimid (Lenalidomide, CC-5013) and CC-4047 are IMiDs immunomodulatory drugs that have been described as having immunomodulatory properties and anti-tumor activity. Here we report proapoptotic effects of CC-5013 and CC-4047 on tumor cells in a co-culture model of PBMC and tumor cells. CC-5013 and CC-4047 enhanced PBMC activity leading to tumor cell apoptosis in K562/PBMC co-culture model. We also demonstrate that the natural killer (NK) cell population of PBMC was essential in inducing K562 apoptosis. Increases of NK and natural killer T (NKT) cell populations by CC-5013 and CC-4047 was observed along with modulation of NK cell CD56 adhesion marker. In addition, our data indicate that NK activation by CC-4047 was dependent on other cell types of PBMC. We expanded the application of K562/PBMC co-culture model to other hematological and solid tumors. In Raji/PBMC co-culture model, CC-5013 and CC-4047 dose-dependently augmented tumor cell apoptosis. Pre-treatment of Raji cells with Rituximab further enhanced apoptosis induced by CC-5013 or CC-4047-treated PBMC. Moreover, CC-5013 and CC-4047 significantly increased PC-3 prostate cancer cell apoptosis in PC-3/PBMC co-culture, either as single agent or in combination with Docetaxel. Together, the results reveal that co-culture models are suitable cellular systems to assess anti-tumor activities of these compounds. Our findings support clinical evaluation of CC-5013 and CC-4047 in relapsed NHL with Rituximab and in prostate cancer with Docetaxel.

摘要

来那度胺(瑞复美,CC - 5013)和CC - 4047是免疫调节药物(IMiDs),已被描述为具有免疫调节特性和抗肿瘤活性。在此,我们报告了CC - 5013和CC - 4047在PBMC与肿瘤细胞的共培养模型中对肿瘤细胞的促凋亡作用。在K562/PBMC共培养模型中,CC - 5013和CC - 4047增强了PBMC活性,导致肿瘤细胞凋亡。我们还证明,PBMC中的自然杀伤(NK)细胞群体在诱导K562凋亡中至关重要。观察到CC - 5013和CC - 4047使NK和自然杀伤T(NKT)细胞群体增加,同时NK细胞CD56黏附标志物也发生了调节。此外,我们的数据表明,CC - 4047对NK的激活依赖于PBMC的其他细胞类型。我们将K562/PBMC共培养模型的应用扩展到了其他血液系统肿瘤和实体瘤。在Raji/PBMC共培养模型中,CC - 5013和CC - 4047剂量依赖性地增强了肿瘤细胞凋亡。用利妥昔单抗预处理Raji细胞进一步增强了CC - 5013或CC - 4047处理的PBMC诱导的凋亡。此外,CC - 5013和CC - 4047在PC - 3/PBMC共培养中显著增加了PC - 3前列腺癌细胞凋亡,无论是作为单一药物还是与多西他赛联合使用。总之,结果表明共培养模型是评估这些化合物抗肿瘤活性的合适细胞系统。我们的研究结果支持对CC - 5013和CC - 4047与利妥昔单抗联合用于复发非霍奇金淋巴瘤(NHL)以及与多西他赛联合用于前列腺癌进行临床评估。

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