Journal
MOLECULAR MEDICINE REPORTS
Volume 11, Issue 3, Pages 1573-1581Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.2888
Keywords
phosphatidylinositol 3-kinase/protein kinase B pathway; glucose transporter-1; cancer; radioresistance
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Funding
- National Natural Science Foundation of China [81172562, 81372903]
- Science and Technology Department of Zhejiang Province, China [2009C33026]
- Health Department of Zhejiang Province [2010KYA062, 20098042]
- Department of Education of Zhejiang Province, China [Y201121184]
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The mechanisms underlying cancer radioresistance remain unclear. Several studies have found that increased glucose transporter-1 (GLUT-1) expression is associated with radioresistance. Recently, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway was reported to be involved in the control of GLUT-1 trafficking and activity. Activation of the PI3K/Akt pathway may itself be associated with cancer radioresistance. Thus, increasing attention has been devoted to the effects of modifying the expression of GLUT-1 and the PI3K/Akt pathway on the increase in the radiosensitivity of cancer cells. This review discusses the importance of the association between elevated expression of GLUT-1 and activation of the PI3K/Akt pathway in the development of radioresistance in cancer.
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