Title : Mitochondrial energetic and AKT status mediate metabolic effects and apoptosis of metformin in human leukemic cells.

Pub. Date : 2013 Nov

PMID : 23568147






6 Functional Relationships(s)
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1 Mitochondrial energetic and AKT status mediate metabolic effects and apoptosis of metformin in human leukemic cells. Metformin AKT serine/threonine kinase 1 Homo sapiens
2 Importantly, leukemic cells with high basal AKT phosphorylation, glucose consumption or glycolysis exhibit a markedly reduced induction of the Pasteur effect in response to metformin and are resistant to metformin-induced apoptosis. Metformin AKT serine/threonine kinase 1 Homo sapiens
3 Importantly, leukemic cells with high basal AKT phosphorylation, glucose consumption or glycolysis exhibit a markedly reduced induction of the Pasteur effect in response to metformin and are resistant to metformin-induced apoptosis. Metformin AKT serine/threonine kinase 1 Homo sapiens
4 Accordingly, glucose starvation or treatment with deoxyglucose or an AKT inhibitor induces sensitivity to metformin. Metformin AKT serine/threonine kinase 1 Homo sapiens
5 Overall, metformin elicits reprogramming of intermediary metabolism leading to inhibition of cell proliferation in all leukemic cells and apoptosis only in leukemic cells responding to metformin with AKT phosphorylation and a strong Pasteur effect. Metformin AKT serine/threonine kinase 1 Homo sapiens
6 Overall, metformin elicits reprogramming of intermediary metabolism leading to inhibition of cell proliferation in all leukemic cells and apoptosis only in leukemic cells responding to metformin with AKT phosphorylation and a strong Pasteur effect. Metformin AKT serine/threonine kinase 1 Homo sapiens