Title : SVCT-2 in breast cancer acts as an indicator for L-ascorbate treatment.

Pub. Date : 2013 Mar 21

PMID : 22665050






4 Functional Relationships(s)
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1 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Reactive Oxygen Species solute carrier family 23 member 2 Homo sapiens
2 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Reactive Oxygen Species solute carrier family 23 member 2 Homo sapiens
3 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Reactive Oxygen Species solute carrier family 23 member 2 Homo sapiens
4 These results suggest that functional SVCT-2 sensitizes breast cancer cells to autophagic damage by increasing the L-ascorbate concentration and intracellular ROS production and furthermore, SVCT-2 in breast cancer may act as an indicator for commencing L-ascorbate treatment. Reactive Oxygen Species solute carrier family 23 member 2 Homo sapiens