Beuran Mircea, Negoi Ionut, Paun Sorin, Ion Adriana Daniela, Bleotu Coralia, Negoi Ruxandra Irina, Hostiuc Sorin
Emergency Hospital of Bucharest, Romania; Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.
Emergency Hospital of Bucharest, Romania; Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.
Pancreatology. 2015 May-Jun;15(3):217-25. doi: 10.1016/j.pan.2015.02.011. Epub 2015 Mar 7.
BACKGROUND/OBJECTIVES: The present article summarizes and analyzes the current knowledge about the role of the epithelial to mesenchymal transition (EMT) in the systemic invasiveness of pancreatic cancer.
An electronic search of PubMed/MEDLINE, EMBASE, and the Web of Science was used to identify relevant original articles and reviews.
The EMT represents a key step during normal embryogenesis. However, increasing evidence reveals its essential role in the local progression and metastasis of pancreatic cancer. Areas of interest are the cross-linking between cells undergoing the EMT and pancreatic cancer stem cells, and the correlation between the EMT and chemoresistance to standard therapies. During carcinogenesis, malignant pancreatic cells at the primary site acquire the ability to undergo the EMT, a transformation associated with increased mobility. The reverse process at secondary sites, the mesenchymal to epithelial transition (MET), has devastating consequences, allowing neoplastic epithelial cells to invade surrounding tissues and spread to distant sites. Consequences of the EMT are the loss of E-cadherin expression and the acquisition of mesenchymal markers including fibronectin or vimentin. Detailed knowledge of the molecular processes underlying the EMT has opened possibilities for new therapeutic agents. These include an EMT approach for patients with early cancers, to prevent invasion and dissemination, and anti-MET therapy for patients with established metastasis.
The current literature shows a strong correlation between the EMT and the systemic aggressiveness of pancreatic tumors. Individualized therapy, targeting the process of EMT and its cross-linking with cancer stem cells, may increase survival of patients with pancreatic cancer.
背景/目的：本文总结并分析了目前关于上皮-间质转化（EMT）在胰腺癌全身侵袭性中作用的相关知识。
通过对PubMed/MEDLINE、EMBASE和科学网进行电子检索，以识别相关的原始文章和综述。
EMT是正常胚胎发育过程中的关键步骤。然而，越来越多的证据表明其在胰腺癌局部进展和转移中起着重要作用。关注的领域包括经历EMT的细胞与胰腺癌干细胞之间的交联，以及EMT与对标准疗法的化疗耐药性之间的相关性。在致癌过程中，原发部位的恶性胰腺细胞获得了发生EMT的能力，这种转变与细胞迁移能力增强有关。在继发部位的相反过程，即间质-上皮转化（MET），会产生毁灭性后果，使肿瘤上皮细胞能够侵入周围组织并扩散到远处部位。EMT的后果是E-钙黏蛋白表达丧失以及获得包括纤连蛋白或波形蛋白在内的间质标志物。对EMT潜在分子过程的详细了解为新型治疗药物开辟了可能性。这些包括针对早期癌症患者的EMT方法，以防止侵袭和扩散，以及针对已发生转移患者的抗MET治疗。
当前文献表明EMT与胰腺肿瘤的全身侵袭性之间存在密切关联。针对EMT过程及其与癌症干细胞交联的个体化治疗可能会提高胰腺癌患者的生存率。
