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DNA Repair (Amst). 2014 Oct;22:24-9. doi: 10.1016/j.dnarep.2014.07.001. Epub 2014 Aug 1.

Akt and p53R2, partners that dictate the progression and invasiveness of cancer.

Author information

1
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
2
Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
3
Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: Ahmadi.bchemistry@yahoo.com.

Abstract

The serine/threonine kinase or the so-called "Akt" is a key regulatory molecule of signaling pathway that regulates various cellular processes. Many intracellular proteins are involved in the activation or inhibition of Akt signaling and the hyperactivation of Akt signaling pathway is found to be frequently involved in various types of human cancers. Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy. In this review article, we will discuss the situation in which cancer cells with hyperactive PI3K/Akt signaling can recruit p53R2 in favor of cancer progression and resistance to therapy. In the hyperactive state of PI3K/Akt signaling (which happens in the absence of deactivation or excess of activation), p53R2 can be used by cancer cells to promote proliferation. Therefore, the hyperactivity of PI3K/Akt pathway and elevated levels of p53R2 can give rise to highly invasive cancers.

KEYWORDS:

Akt; Cancer progression; Cell cycle; P53R2; Ribonucleotide reductase

PMID:
25086499
DOI:
10.1016/j.dnarep.2014.07.001
[Indexed for MEDLINE]

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