自噬
MAPK/ERK通路
p38丝裂原活化蛋白激酶
细胞生物学
细胞凋亡
生物
激酶
细胞外
细胞应激反应
癌症研究
信号转导
蛋白激酶A
战斗或逃跑反应
生物化学
基因
作者
Xinbing Sui,Na Kong,Li Ye,Weidong Han,Jichun Zhou,Qin Zhang,Chao He,Hongming Pan
出处
期刊:Cancer Letters
[Elsevier]
日期:2013-12-11
卷期号:344 (2): 174-179
被引量:829
标识
DOI:10.1016/j.canlet.2013.11.019
摘要
The Mitogen Activated Protein Kinase (MAPK) signaling plays a critical role in the outcome and the sensitivity to anticancer therapies. Activated MAPK can transmit extracellular signals to regulate cell growth, proliferation, differentiation, migration, apoptosis and so on. Apoptosis as well as macroautophagy (hereafter referred to as autophagy) can be induced by extracellular stimuli such the treatment of chemotherapeutic agents, resulting in different cell response to these drugs. However, the molecular mechanisms mediating these two cellular processes remain largely unknown. Recently, several studies provide new insights into p38 and JNK MAPK pathways function in the control of the balance of autophagy and apoptosis in response to genotoxic stress. Our increased understanding of the role of p38 and JNK MAPK pathways in regulating the balance of autophagy and apoptosis will hopefully provide prospective strategies for cancer therapy.
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