Metabolomic and Mitochondrial Fingerprinting of the Epithelial-to-Mesenchymal Transition (EMT) in Non-Tumorigenic and Tumorigenic Human Breast Cells.

In the latter regard, it should be noted that a significant alteration in the electron flow intensity from succinate to mitochondrial complex II and III was indirectly confirmed in saponin-permeabilized tumorigenic EMT cells, in which the mitochondria functioning exhibited partial resistance to respiratory complex II inhibitors and a highly significant refractoriness to complex III inhibitors.

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