|
Review
Phosphatidylinositide 3-kinase/AKT
in radiation responses
M. Zhan and Z.C. Han
State key Laboratory of Experimental Hematology,
Institute of Hematology, National Research Center of Stem Cell
Engineering and Technology, Institute of Hematology & Hospital
of Blood Diseases, Chinese Academy of Medical Sciences and Peking
Union of Medical Colleges, Tianjin, China
Offprint requests to: Dr. Mei Zhan, State Key Laboratory of
Experimental Hematology, Institute of Hematology, National Research
Center of Stem cell Engineering and Technology, Institute of
Hematology and Hospital of Blood Diseases, Chinese Academy of
Medical Sciences and Peking Union of Medical Colleges, Tiangin
30020, China.
Summary. 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. Histol. Histopathol.
19, 915-923 (2004)
Key words: Radiation,
Phosphatidylinositide 3-kinase, Signal transduction, Cross-talk
DOI: 10.14670/HH-19.915
|