Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Global COE 'Cell Fate Regulation Research and Education Unit', Kumamoto University, 5-1 Oe-honmachi, Kumamoto 862-0973, Japan.
Int J Oncol. 2012 Apr;40(4):1071-8. doi: 10.3892/ijo.2011.1313. Epub 2011 Dec 20.
Primary effusion lymphoma (PEL) is a subtype of B-cell lymphoma caused by human herpes virus 8/Kaposi sarcoma-associated herpes virus (HHV-8/KSHV), which is mostly found in patients with AIDS and has poor prognosis. Nuclear factor (NF)-κB pathway is constitutively activated in HHV-8-infected PEL cells and plays a crucial role in tumorigenesis. Recently, it has been shown that diethyldithiocarbamate (DDTC), an active metabolite of disulfiram, has apoptotic activity in cancer cells. Here, we investigated the effect of DDTC on PEL using a PEL mouse model generated by intraperitoneal injection of BC-3 cells, a PEL cell line. DDTC ameliorated the symptoms of PEL in these mice, such as development of ascites, splenomegaly and increase of body weight, in comparison with PBS-treated controls. Moreover, we determined in vitro that DDTC suppressed the constitutively activated NF-κB pathway in BC-3 cells. Methylthiotetrazole assay revealed that the cell proliferation of various PEL cell lines was significantly suppressed by the treatment of DDTC. DDTC also induced the expression of cleaved caspase-3, an apoptosis marker, whereas the addition of Q-VD-OPh, a pan-caspase inhibitor, inhibited cell apoptosis induced by DDTC treatment. Together, our results indicated that DDTC induces apoptosis via inhibition of the NF-κB signaling pathway in HHV-8-infected PEL cells. This study suggests the potential use of DDTC as a therapeutic approach for PEL.
原发性渗出性淋巴瘤(PEL)是一种由人类疱疹病毒 8/卡波西肉瘤相关疱疹病毒(HHV-8/KSHV)引起的 B 细胞淋巴瘤亚型,主要发生在艾滋病患者中,预后不良。HHV-8 感染的 PEL 细胞中核因子(NF)-κB 通路持续激活,在肿瘤发生中发挥关键作用。最近,已经表明二乙基二硫代氨基甲酸盐(DDTC)是二硫化四乙基秋兰姆的活性代谢物,在癌细胞中具有凋亡活性。在这里,我们使用腹腔注射 PEL 细胞系 BC-3 细胞生成的 PEL 小鼠模型研究了 DDTC 对 PEL 的影响。与 PBS 处理的对照组相比,DDTC 改善了这些小鼠的 PEL 症状,例如腹水、脾肿大和体重增加。此外,我们在体外确定 DDTC 抑制了 BC-3 细胞中持续激活的 NF-κB 通路。甲基噻唑四唑测定表明,DDTC 处理显著抑制了各种 PEL 细胞系的细胞增殖。DDTC 还诱导了 cleaved caspase-3 的表达,这是一种凋亡标志物,而添加 pan-caspase 抑制剂 Q-VD-OPh 抑制了 DDTC 处理诱导的细胞凋亡。总之,我们的结果表明,DDTC 通过抑制 HHV-8 感染的 PEL 细胞中的 NF-κB 信号通路诱导细胞凋亡。这项研究表明,DDTC 作为治疗 PEL 的一种潜在方法具有潜力。