Showalter Shayna L, Huang Yu-Hung, Witkiewicz Agneszka, Costantino Christina L, Yeo Charles J, Green Jordan J, Langer Robert, Anderson Daniel G, Sawicki Janet A, Brody Jonathan R
Department of Surgery, Thomas Jefferson Pancreas, Biliary and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Cancer Biol Ther. 2008 Oct;7(10):1584-90. doi: 10.4161/cbt.7.10.6562. Epub 2008 Oct 3.
Pancreatic cancer is the fourth leading cause of cancer-related deaths in this country, and there is currently no effective targeted treatment for this deadly disease. A dire need exists to rapidly translate our molecular understanding of this devastating disease into effective, novel therapeutic options. Mesothelin is a candidate target protein shown by a number of laboratories to be specifically overexpressed in pancreatic cancers and not in the adjacent normal tissue. Translational investigations have shown promising results using this molecule as a therapeutic target (e.g., vaccine strategies). In addition, the mesothelin promoter has been cloned and dissected and can therefore be used as a vehicle for regulating expression of DNA sequences. Using a novel, proven, biodegradable nanoparticulate system, we sought to target mesothelin-expressing pancreatic cancer cells with a potent suicide gene, diphtheria toxin-A (DT-A). We first confirmed reports that a majority of pancreatic cancer cell lines and resected pancreatic ductal adenocarcinoma specimens overexpressed mesothelin at the mRNA and protein levels. High mesothelin-expressing pancreatic cancer cell lines produced more luciferase than cell lines with undetectable mesothelin expression when transfected with a luciferase sequence under the regulation of the mesothelin promoter. We achieved dramatic inhibition of protein translation (>95%) in mesothelin-expressing pancreatic cancer cell lines when DT-A DNA, driven by the mesothelin promoter, was delivered to pancreatic cancer cells. We show that this inhibition effectively targets the death of pancreatic cancer cells that overexpress mesothelin. The work presented here provides evidence that this strategy will work in pre-clinical mouse pancreatic cancer models, and suggests that such a strategy will work in the clinical setting against the majority of pancreatic tumors, most of which overexpress mesothelin.
胰腺癌是该国癌症相关死亡的第四大主要原因,目前对于这种致命疾病尚无有效的靶向治疗方法。迫切需要将我们对这种毁灭性疾病的分子理解迅速转化为有效的新型治疗选择。间皮素是一种候选靶蛋白,许多实验室已证明其在胰腺癌中特异性过表达,而在相邻的正常组织中则不表达。转化研究表明,将该分子用作治疗靶点(例如疫苗策略)已取得了有前景的结果。此外,间皮素启动子已被克隆和剖析,因此可作为调节DNA序列表达的载体。我们使用一种新型、经过验证的可生物降解纳米颗粒系统,试图用一种强效自杀基因——白喉毒素A(DT-A)靶向表达间皮素的胰腺癌细胞。我们首先证实了之前的报道,即大多数胰腺癌细胞系和切除的胰腺导管腺癌标本在mRNA和蛋白质水平上过表达间皮素。当用间皮素启动子调控的荧光素酶序列转染时,高表达间皮素的胰腺癌细胞系产生的荧光素酶比间皮素表达不可检测的细胞系更多。当由间皮素启动子驱动的DT-A DNA被递送至胰腺癌细胞时,我们在表达间皮素的胰腺癌细胞系中实现了对蛋白质翻译的显著抑制(>95%)。我们表明这种抑制有效地靶向了过表达间皮素的胰腺癌细胞的死亡。此处展示的工作提供了证据,表明该策略在临床前小鼠胰腺癌模型中可行,并表明这种策略在临床环境中对大多数胰腺肿瘤有效,其中大多数肿瘤过表达间皮素。