Title : Effects of sorafenib on energy metabolism in breast cancer cells: role of AMPK-mTORC1 signaling.

Pub. Date : 2013 Aug

PMID : 23963659






5 Functional Relationships(s)
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1 This previously unrecognized long-term effect of sorafenib was mediated by AMPK-dependent inhibition of the mTORC1 pathway. Sorafenib CREB regulated transcription coactivator 1 Mus musculus
2 Suppression of mTORC1 activity was sufficient for sorafenib to hinder glucose utilization in breast cancer cells, as demonstrated by the observation that the mTORC1 inhibitor rapamycin induced a comparable down-regulation of GLUT-1 expression and glucose uptake. Sorafenib CREB regulated transcription coactivator 1 Mus musculus
3 Suppression of mTORC1 activity was sufficient for sorafenib to hinder glucose utilization in breast cancer cells, as demonstrated by the observation that the mTORC1 inhibitor rapamycin induced a comparable down-regulation of GLUT-1 expression and glucose uptake. Sorafenib CREB regulated transcription coactivator 1 Mus musculus
4 The key role of AMPK-dependent inhibition of mTORC1 in sorafenib mechanisms of action was confirmed by AMPKalpha1 silencing, which restored mTORC1 activity conferring a significant protection from cell death. Sorafenib CREB regulated transcription coactivator 1 Mus musculus
5 The key role of AMPK-dependent inhibition of mTORC1 in sorafenib mechanisms of action was confirmed by AMPKalpha1 silencing, which restored mTORC1 activity conferring a significant protection from cell death. Sorafenib CREB regulated transcription coactivator 1 Mus musculus