Zhu Dan, Corral Laura G, Fleming Yuedi W, Stein Bernd
Celgene Corporation, 4550 Towne Centre Court, San Diego, CA, 92121, USA.
Cancer Immunol Immunother. 2008 Dec;57(12):1849-59. doi: 10.1007/s00262-008-0512-7. Epub 2008 Apr 8.
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.
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。