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Published Erratum
. 2018 Jun:16:426-427.
doi: 10.1016/j.redox.2018.03.001. Epub 2018 Mar 13.

Corrigendum to 'A review of the basics of mitochondrial bioenergetics, metabolism, and related signaling pathways in cancer cells: Therapeutic targeting of tumor mitochondria with lipophilic cationic compounds' [REDOX 14C (2017) 316-327]

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Published Erratum

Corrigendum to 'A review of the basics of mitochondrial bioenergetics, metabolism, and related signaling pathways in cancer cells: Therapeutic targeting of tumor mitochondria with lipophilic cationic compounds' [REDOX 14C (2017) 316-327]

Balaraman Kalyanaraman et al. Redox Biol. 2018 Jun.
No abstract available

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Figures

Fig. 5
Fig. 5
Inhibition of cell proliferation by 2-DG and metformin, and synergistic depletion of ATP by 2-DG and metformin in MiaPaCa-2 cells. (A) Effects of 2-DG and metformin alone and together, on cell proliferation. MiaPaCa-2 and Capan-2 cells were treated with 2-DG (0.5 mM in MiaPaCa-2, 1 mM in Capan-2 cells) or metformin (1 mM) alone and together. Cell proliferation was monitored in real time with the continuous presence of indicated treatments until the end of each experiment. The changes in cell confluence are used as a surrogate marker of cell proliferation. Data shown are the mean ± SD. (n = 6). (B–D) MiaPaCa-2 cells were treated with 2-DG (0.3–3 mM) or metformin (0.3–30 mM) independently and together for 6 h (B) or 24 h (D) and intracellular ATP levels were determined, normalized to total cellular protein amount, and expressed as percentage of untreated cells. A three-dimensional representation showing the concentration-dependent effects of 2-DG or metformin alone and together on intracellular ATP levels in MiaPaCa-2 cells. The combination index-fraction affected (CI-Fa) plots are shown (C,E). Fraction affected parameter is used as a measure of the drug(s) efficiency, with a value of zero indicating the lack of effect on intracellular ATP and the value of 1 indicating total depletion of intracellular ATP. (Obtained from Ref. [43], Copyright © 2014, Rights Managed by Nature Publishing Group).

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