期刊
CELL ADHESION & MIGRATION
卷 9, 期 4, 页码 317-324出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/19336918.2015.1016686
关键词
anti-cancer therapy; EMT; extracellular matrix; PI3K; Akt signaling pathway; transcription factors; tumor aggressiveness; EMT; epithelial-mesenchymal transition; PI3K; phosphatidylinositol-3-kinase; PKA; protein kinase A; PKC; protein kinase C; PKB; protein kinase B; PDK1; 3-phosphoinositide-dependent protein kinase 1; CK; cytokeratin; bHLH; basic helix-loop-helix protein; YB-1; Y-box binding protein-1; MET; mesenchymal-epithelial transition; GSK-3; glycogen synthase kinase 3; ILK; integrin-linked kinase; ECM; extracellular matrix; PDGF; platelet-derived growth factor; FGF; fibroblast growth factor; TGF-; transforming growth factor-; TNF-; tumor necrosis factor-; MDR; multidrug resistance
类别
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据