Division of Oncology Research, Department of Medicine, Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.
World J Gastroenterol. 2012 Oct 14;18(38):5321-3. doi: 10.3748/wjg.v18.i38.5321.
Pancreatic cancer is the deadliest solid cancer and currently the fourth most frequent cause of cancer-related deaths. Emerging evidence suggests that cancer stem cells (CSCs) play a crucial role in the development and progression of this disease. The identification of CSC markers could lead to the development of new therapeutic targets. In this study, the authors explore the functional role of c-Met in pancreatic CSCs, by analyzing self-renewal with sphere assays and tumorigenicity capacity in NOD SCID mice. They concluded that c-Met is a novel marker for identifying pancreatic CSCs and c-Met(high) in a higher tumorigenic cancer cell population. Inhibition of c-Met with XL184 blocks self-renewal capacity in pancreatic CSCs. In pancreatic tumors established in NOD SCID mice, c-Met inhibition slowed tumor growth and reduced the population of CSCs, along with preventing the development of metastases.
胰腺癌是最致命的实体瘤,目前是癌症相关死亡的第四大主要原因。新出现的证据表明,癌症干细胞 (CSC) 在这种疾病的发展和进展中起着至关重要的作用。CSC 标志物的鉴定可能会导致新的治疗靶点的开发。在这项研究中,作者通过分析球体试验中的自我更新和 NOD SCID 小鼠的致瘤能力,探讨了 c-Met 在胰腺 CSC 中的功能作用。他们得出结论,c-Met 是鉴定胰腺 CSC 的新标志物,c-Met(高)在更高致瘤性的癌细胞群体中。用 XL184 抑制 c-Met 可阻断胰腺 CSC 的自我更新能力。在 NOD SCID 小鼠中建立的胰腺肿瘤中,c-Met 抑制减缓了肿瘤生长并减少了 CSC 群体,同时防止了转移的发展。