Impacts of activation of the mitogen-activated protein kinase pathway in pancreatic cancer

被引:46
|
作者
Furukawa, Toru [1 ]
机构
[1] Tokyo Womens Med Univ, Inst Integrated Med Sci, Tokyo 1628666, Japan
来源
FRONTIERS IN ONCOLOGY | 2015年 / 5卷
关键词
pancreatic cancer; mitogen-activated protein kinase; KRAS; BRAF; DUSP6; ERK; MKP-3; microRNA; SUPPRESSES TUMOR-GROWTH; CELL-CYCLE PROGRESSION; GENE-EXPRESSION; INTRAEPITHELIAL NEOPLASIA; PHOSPHATASE; TARGETS; DUSP6; BRAF; IDENTIFICATION; DUSP6/MKP-3;
D O I
10.3389/fonc.2015.00023
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Pancreatic cancer is characterized by constitutive activation of the mitogen-activated protein kinase (MARK) pathway. Mutations of KRAS or BRAF and epigenetic abrogation of DUSP6 contribute synergistically to the constitutive activation of MARK. Active MARK induces the expression of a variety of genes that are thought to play roles in malignant phenotypes of pancreatic cancer. By blocking the functions of such induced genes, it is possible to attenuate the malignant phenotypes.The development of drugs targeting genes downstream of MARK may provide a novel therapeutic option for pancreatic cancer.
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页数:5
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