c-Met in pancreatic cancer stem cells: Therapeutic implications
c-Met in pancreatic cancer stem cells: Therapeutic implications
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DOI：
10.3748/wjg.v18.i38.5321
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发表时间：
2012-10-14
影响因子：
4.3
通讯作者：
Bujanda, Luis
中科院分区：
文献类型：
--
作者：
Herreros-Villanueva, Marta;Zubia-Olascoaga, Aizpea;Bujanda, Luis
胰腺癌是最致命的实体癌，目前是癌症相关死亡的第四大常见原因。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标志物的鉴定可能导致新的治疗靶点的开发。在这项研究中，作者通过分析NOD SCID小鼠的球体试验和致瘤能力的自我更新，探索了c-Met在胰腺CSC中的功能作用。他们得出结论，c-Met是一种新的标记物，用于在较高致瘤性的癌细胞群中识别胰腺CSC和c-Met（高）。用XL 184抑制c-Met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，沿着防止了转移的发展。(C)2012年百世登。All rights reserved.
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. (C) 2012 Baishideng. All rights reserved.