Title : Sorafenib induces cathepsin B-mediated apoptosis of bladder cancer cells by regulating the Akt/PTEN pathway. The Akt inhibitor, perifosine, enhances the sorafenib-induced cytotoxicity against bladder cancer cells.

Pub. Date : 2015

PMID : 26097873






6 Functional Relationships(s)
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1 Sorafenib induces cathepsin B-mediated apoptosis of bladder cancer cells by regulating the Akt/PTEN pathway. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
2 The Akt inhibitor, perifosine, enhances the sorafenib-induced cytotoxicity against bladder cancer cells. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
3 Moreover, we found that cathepsin B enzymatic activity, induced by sorafenib, is dependent on its dephosphorylation via PTEN activation and Akt inactivation. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
4 In addition, the Akt inhibitor perifosine increased the sensitivity of bladder cancer cells to sorafenib-induced cytotoxicity. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
5 Overall, our results show that apoptotic cell death induced by sorafenib in bladder cancer cells is dependent on cathepsin B activity and involved PTEN and Akt signaling pathways. Sorafenib AKT serine/threonine kinase 1 Homo sapiens
6 The Akt inhibitor perifosine increased the cytotoxic effects of sorafenib in bladder cancer cells. Sorafenib AKT serine/threonine kinase 1 Homo sapiens