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AKT as Locus of Cancer Phenotype
Author(s) -
Radisavljevic Ziv
Publication year - 2015
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24947
Subject(s) - protein kinase b , phenotype , locus (genetics) , cancer research , pi3k/akt/mtor pathway , biology , gene , phosphorylation , signal transduction , genetics
Cancer robustness is generated by the positive feedback loops. The positive loops hyperactivate AKT locus forming a cancer phenotype in leukemia, lymphoma, myeloma, plasmocytoma, sarcoma and carcinoma. The positive loops inducing AKT hyperphosphorylation increase activity of the AKT locus and the nodal associated and interconnected signaling genes. Only genes expressed above the threshold in the AKT signaling interactome networks, participate in the formation of the complex cancer phenotype. AKT is the switching locus for the cancer phenotype. The phenotype formation and maintenance is regulated by the AKT locus through an entropy/enthalpy processes. Targeting the AKT by locus chemotherapy, changing redox balance (antioxidant/oxidant), affects phosphorylation and activity of the AKT, inducing conversion of the positive feedback loops and disappearance of the malignant phenotype. J. Cell. Biochem. 116: 1–5, 2015. © 2014 Wiley Periodicals, Inc.