Title : Activation of phosphatidylinositol 3-kinase/AKT/snail signaling pathway contributes to epithelial-mesenchymal transition-induced multi-drug resistance to sorafenib in hepatocellular carcinoma cells.

Pub. Date : 2017

PMID : 28934275






5 Functional Relationships(s)
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1 Activation of phosphatidylinositol 3-kinase/AKT/snail signaling pathway contributes to epithelial-mesenchymal transition-induced multi-drug resistance to sorafenib in hepatocellular carcinoma cells. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
2 The activation of AKT by sorafenib is thought to be responsible for the development of these characteristics. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
3 Two sorafenib-resistant HCC cell lines, established from human HCC HepG2 and Huh7 cells, were refractory to sorafenib-induced growth inhibition but were sensitive to MK-2206, a novel allosteric AKT inhibitor. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
4 Thus, the combination of sorafenib and MK-2206 led to significant reversion of the EMT phenotype and P-gp-mediated MDR by downregulating phosphorylated AKT. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
5 These findings underscore the significance of EMT, MDR and enhanced PI3K/AKT signaling in sorafenib-resistant HCC cells. Sorafenib AKT serine/threonine kinase 1 Homo sapiens