Sodium orthovanadate (SOV) is an inhibitor of protein tyrosine phosphatases, alkaline phosphatases and a number of ATPases, most likely acting as a phosphate analogue[3]. The decreased tyrosine phosphorylation of PTEN and the decreased serine phosphorylation of Akt induced by ischemia were suppressed by SOV, respectively. SOV could alter the phosphorylation status of ASK1 at serine 83 and threonine 845 induced by ischemia[4]. SOV changed SFA (saturated fatty acids) and MUFA (monounsaturated fatty acids) composition in THP-1 macrophages and increased expression of SCD (stearoyl-coenzyme A desaturase). Sodium orthovanadate did not affect the amount of any PUFA[5]. SOV is able to overcome sorafenib resistance and strengthens sorafenib in suppressing sorafenib-resistant HCC (hepatocellular carcinoma) cells in vitro and in animal models. Similar to its action on parental HCC cells, SOV induced cell cycle arrest at G2/M phases by regulating cyclin B1 and cyclin-dependent kinase 1, and apoptosis by reducing mitochondrial membrane potential, in sorafenib-resistant HCC cells[6].
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