Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/26496
Title: The phosphatidylinositol 3-kinase/Akt and c-Jun N-terminal kinase signaling in cancer: Alliance or contradiction? (Review)
Authors: Zhao, HF
Wang, J
To, SST 
Keywords: Apoptosis
Crosstalk
EGFR
JNK
PI3K/Akt
PTEN
Tumor development
Issue Date: 2015
Publisher: Spandidos Publications
Source: International journal of oncology, 2015, v. 47, no. 2, p. 429-436 How to cite?
Journal: International journal of oncology 
Abstract: The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway and c-Jun N-terminal kinase (JNK) pathway are responsible for regulating a variety of cellular processes including cell growth, migration, invasion and apoptosis. These two pathways are essential to the development and progression of tumors. The dual roles of JNK signaling in apoptosis and tumor development determine the different interactions between the PI3K/Akt and JNK pathways. Activation of PI3K/ Akt signaling can inhibit stress- and cytokine-induced JNK activation through Akt antagonizing and the formation of the JIP1-JNK module, as well as the activities of upstream kinases ASK1, MKK4/7 and MLK. On the other hand, hyperactivation of Akt and JNK is also found in cancers that harbor EGFR overexpression or loss of PTEN. Understanding the activation mechanism of PI3K/Akt and JNK pathways, as well as the interplays between these two pathways in cancer may contribute to the identification of novel therapeutic targets. In the present report, we summarized the current understanding of the PI3K/Akt and JNK signaling networks, as well as their biological roles in cancers. In addition, the interactions and regulatory network between PI3K/Akt and JNK pathways in cancer were discussed.
URI: http://hdl.handle.net/10397/26496
ISSN: 1019-6439
EISSN: 1791-2423
DOI: 10.3892/ijo.2015.3052
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