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丝裂原活化蛋白激酶通路激活在胰腺癌中的影响。

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

作者信息

Furukawa Toru

机构信息

Institute for Integrated Medical Sciences, Tokyo Women's Medical University , Tokyo , Japan.

出版信息

Front Oncol. 2015 Feb 4;5:23. doi: 10.3389/fonc.2015.00023. eCollection 2015.

DOI:10.3389/fonc.2015.00023
PMID:25699241
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4316689/
Abstract

Pancreatic cancer is characterized by constitutive activation of the mitogen-activated protein kinase (MAPK) pathway. Mutations of KRAS or BRAF and epigenetic abrogation of DUSP6 contribute synergistically to the constitutive activation of MAPK. Active MAPK 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 MAPK may provide a novel therapeutic option for pancreatic cancer.

摘要

胰腺癌的特征是丝裂原活化蛋白激酶（MAPK）通路的组成性激活。KRAS或BRAF的突变以及DUSP6的表观遗传缺失协同促成了MAPK的组成性激活。活性MAPK诱导多种基因的表达，这些基因被认为在胰腺癌的恶性表型中发挥作用。通过阻断此类诱导基因的功能，有可能减弱恶性表型。开发针对MAPK下游基因的药物可能为胰腺癌提供一种新的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f39/4316689/dc2b7667c499/fonc-05-00023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f39/4316689/ae6b20d7f078/fonc-05-00023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f39/4316689/dc2b7667c499/fonc-05-00023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f39/4316689/ae6b20d7f078/fonc-05-00023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f39/4316689/dc2b7667c499/fonc-05-00023-g002.jpg

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