Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8310992 | Clinica Chimica Acta | 2015 | 11 Pages |
Abstract
Osteosarcoma (OS) is the most common nonhematologic bone malignancy in children and adolescents. Despite the advances of adjuvant chemotherapy and significant improvement of survival, the prognosis remains generally poor. As such, the search for more effective anti-OS agents is urgent. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is thought to be one of the most important oncogenic pathways in human cancer. An increasing body of evidence has shown that this pathway is frequently hyperactivated in OS and contributes to disease initiation and development, including tumorigenesis, proliferation, invasion, cell cycle progression, inhibition of apoptosis, angiogenesis, metastasis and chemoresistance. Inhibition of this pathway through small molecule compounds represents an attractive potential therapeutic approach for OS. The aim of this review is to summarize the roles of the PI3K/Akt pathway in the development and progression of OS, and to highlight the therapeutic potential of targeting this signaling pathway. Knowledge obtained from the application of these compounds will help in further understanding the pathogenesis of OS and designing subsequent treatment strategies.
Keywords
mTORPDGFRCXCR7IGF1RPDK1ET-1PIP3CSCsHIF-1miRNAsPIP2ETARMMPTNFCDKPI3KNF-κBMdm2RTKsAktOsteosarcomaendothelin A receptorendothelin-1murine double minute 2retinoblastomamicroRNAsCancer stem cellshypoxia-inducible factor-1tumor necrosis factornuclear factor-κBphosphatase and tensin homologphosphatidylinositol 3,4,5-triphosphatePhosphatidylinositol 3-kinasephosphatidylinositol 4,5-biphosphateMatrix metalloproteinase.mammalian target of rapamycinPleckstrin Homologyphosphoinositide-dependent kinase 1Ptencyclin-dependent kinaseGallic acidreceptor tyrosine kinasesplatelet-derived growth factor receptorinsulin-like growth factor 1 receptor
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Authors
Jian Zhang, Xiao-Hua Yu, Yi-Guo Yan, Cheng Wang, Wen-Jun Wang,