Epithelial-mesenchymal transition in pancreatic cancer: Is it a clinically significant factor?

被引:39
|
作者
Jiang, Jia-Hao [1 ,2 ,3 ]
Liu, Chen [1 ,3 ]
Cheng, He [1 ,2 ,3 ]
Lu, Yu [1 ,3 ]
Qin, Yi [1 ,3 ]
Xu, Yong-Feng [1 ,2 ,3 ]
Xu, Jin [1 ,2 ,3 ]
Long, Jiang [1 ,2 ,3 ]
Liu, Liang [1 ,2 ,3 ]
Ni, Quan-Xing [1 ,2 ,3 ]
Yu, Xian-Jun [1 ,2 ,3 ]
机构
[1] Fudan Univ, Shanghai Canc Ctr, Dept Pancreat & Hepatobiliary Surg, Shanghai 200032, Peoples R China
[2] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, PR, Peoples R China
[3] Fudan Univ, Pancreat Canc Inst, Shanghai 200032, PR, Peoples R China
来源
基金
美国国家科学基金会;
关键词
Epithelial-mesenchymal transition; Pancreatic cancer; Tumarigenesis; Metastasis; Prognosis; Therapy; TUMOR-SUPPRESSOR GENE; E-CADHERIN EXPRESSION; DUCTAL ADENOCARCINOMA; DOWN-REGULATION; UP-REGULATION; K-RAS; CELLS; EMT; AUTOPHAGY; SNAIL;
D O I
10.1016/j.bbcan.2014.11.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pancreatic cancer is one of the most aggressive solid malignancies. This aggressiveness is partly attributable to extensive local tumor invasion and early systemic dissemination as well as resistance to chemotherapy. Epithelial mesenchymal transition (EMT) plays fundamental roles in embryonic development and in the differentiation of normal tissues and organs. EMT also plays critical roles in tumor formation, dissemination and drug resistance in pancreatic cancer. Emerging data suggest that inhibiting EMT may reverse the EMT phenotype and enhance the efficacy of chemotherapeutic agents against pancreatic cancer cells. Thus, an understanding of the molecular biology of EMT in pancreatic cancer may provide insights into the mechanisms of tumor invasion and metastatic progression and facilitate the development of alternative therapeutic approaches to improve the treatment outcomes for patients suffering from pancreatic cancer. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:43 / 49
页数:7
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