| Literature DB >> 26241004 |
Wenting Xu1, Zhen Yang, Nonghua Lu.
Abstract
Tumor metastasis is not only a sign of disease severity but also a major factor causing treatment failure and cancer-related death. Therefore, studies on the molecular mechanisms of tumor metastasis are critical for the development of treatments and for the improvement of survival. The epithelial-mesenchymal transition (EMT) is an orderly, polygenic biological process that plays an important role in tumor cell invasion, metastasis and chemoresistance. The complex, multi-step process of EMT involves multiple regulatory mechanisms. Specifically, the PI3K/Akt signaling pathway can affect the EMT in a variety of ways to influence tumor aggressiveness. A better understanding of the regulatory mechanisms related to the EMT can provide a theoretical basis for the early prediction of tumor progression as well as targeted therapy.Entities:
Keywords: CK, cytokeratin; ECM, extracellular matrix; EMT; EMT, epithelial-mesenchymal transition; FGF, fibroblast growth factor; GSK-3β, glycogen synthase kinase 3 β; ILK, integrin-linked kinase; MDR, multidrug resistance; MET, mesenchymal-epithelial transition; PDGF, platelet-derived growth factor; PDK1, 3-phosphoinositide-dependent protein kinase 1; PI3K, phosphatidylinositol-3-kinase; PI3K/Akt signaling pathway; PKA, protein kinase A; PKB, protein kinase B; PKC, protein kinase C; TGF-β, transforming growth factor-β; TNF-α, tumor necrosis factor-α; YB-1, Y-box binding protein-1; anti-cancer therapy; bHLH, basic helix-loop-helix protein; extracellular matrix; transcription factors; tumor aggressiveness
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Year: 2015 PMID： 26241004 PMCID： PMC4594353 DOI： 10.1080/19336918.2015.1016686
Source DB: PubMed Journal: Cell Adh Migr ISSN： 1933-6918 Impact factor: 3.405