Title : Dual inhibition of Akt and c-Met as a second-line therapy following acquired resistance to sorafenib in hepatocellular carcinoma cells.

Pub. Date : 2017 Mar

PMID : 28164434






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1 Dual inhibition of Akt and c-Met as a second-line therapy following acquired resistance to sorafenib in hepatocellular carcinoma cells. Sorafenib MET proto-oncogene, receptor tyrosine kinase Homo sapiens
2 In this study, sorafenib-resistant HCC cells generated from sorafenib-sensitive human HCC cells were shown to overproduce hepatocyte growth factor (HGF) and overexpress c-Met kinase and its phosphorylated form, leading to the activation of Akt and ERK (extracellular signaling-regulated kinase) pathways. Sorafenib MET proto-oncogene, receptor tyrosine kinase Homo sapiens
3 In this study, sorafenib-resistant HCC cells generated from sorafenib-sensitive human HCC cells were shown to overproduce hepatocyte growth factor (HGF) and overexpress c-Met kinase and its phosphorylated form, leading to the activation of Akt and ERK (extracellular signaling-regulated kinase) pathways. Sorafenib MET proto-oncogene, receptor tyrosine kinase Homo sapiens
4 Use of specific c-Met inhibitors enhanced the effects of sorafenib by inhibiting the growth of sorafenib-resistant HCC cells. Sorafenib MET proto-oncogene, receptor tyrosine kinase Homo sapiens
5 Use of specific c-Met inhibitors enhanced the effects of sorafenib by inhibiting the growth of sorafenib-resistant HCC cells. Sorafenib MET proto-oncogene, receptor tyrosine kinase Homo sapiens
6 Akt inhibitors, a class of second-line therapeutic drugs under investigation for treating HCC in clinical trials, enhanced the effects of sorafenib, but also activated the c-Met pathway in sorafenib-resistant cells. Sorafenib MET proto-oncogene, receptor tyrosine kinase Homo sapiens
7 These results provide strong evidence for further investigation on the clinical utility of dual inhibition of Akt and c-Met, particularly MK2206 and capmatinib, as a second-line therapy for advanced HCC that has acquired resistance to sorafenib. Sorafenib MET proto-oncogene, receptor tyrosine kinase Homo sapiens