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Histol Histopathol. 2004 Jul;19(3):915-23.

Phosphatidylinositide 3-kinase/AKT in radiation responses.

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  • 1State key Laboratory of Experimental Hematology, Institute of Hematology, National Research Center of Stem Cell Engineering and Technology, Hospital of Blood Diseases, Chinese Academy of Medical Sciences, Tianjin, China.


Ionizing or ultraviolet radiation-induced cellular survival signaling pathways induce development of cancer and insensitivity of tumor cells to radiation therapy. Accumulating evidence suggests that the phosphatidylinositide 3-kinase (PI3K)/AKT signal pathway is a major contributor to radioresistance. In many cell types PI3K/AKT signaling is a key cytoprotective response downstream of the EGFR family receptors and mediated carcinogenesis. Cytokines, such as HGF, IGF-I, and IL-6 also protects cells against apoptosis induced by radiation through PI3K/AKT pathway. The mechanics by which PI3K/AKT signaling functions in radiation responses may include its regulation of mitochondrial proteins, transcription factors, translation machinery, and cell-cycle progression. In addition, cross-talk between the PI3K/AKT pathway and mitogen-activated protein kinases, protein kinase A, and protein kinase C signal pathway may also play an important role.

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