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Int. J. Mol. Sci. 2015, 16(9), 21138-21152; doi:10.3390/ijms160921138

PI3K and AKT: Unfaithful Partners in Cancer

Department of Visceral Surgery, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Pavillon 4, Av. de Beaumont, Lausanne 1011, Switzerland
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Author to whom correspondence should be addressed.
Academic Editor: William Chi-shing Cho
Received: 25 July 2015 / Revised: 28 August 2015 / Accepted: 1 September 2015 / Published: 3 September 2015
(This article belongs to the Collection Advances in Molecular Oncology)
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Abstract

The phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway regulates multiple cellular processes. An overactivation of the pathway is frequently present in human malignancies and plays a key role in cancer progression. Hence, its inhibition has become a promising approach in cancer therapy. However, the development of resistances, such as the abrogation of negative feedback mechanisms or the activation of other proliferative signaling pathways, has considerably limited the anticancer efficacy of PI3K/AKT inhibitors. In addition, emerging evidence points out that although AKT is acknowledged as the major downstream effector of PI3K, both PI3K and AKT can operate independently of each other in cancer, revealing another level of complexity in this pathway. Here, we highlight the complex relationship between PI3K and AKT in cancer and further discuss the consequences of this relationship for cancer therapy. View Full-Text
Keywords: cancer; signaling; PI3K; AKT; therapies cancer; signaling; PI3K; AKT; therapies
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Faes, S.; Dormond, O. PI3K and AKT: Unfaithful Partners in Cancer. Int. J. Mol. Sci. 2015, 16, 21138-21152.

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