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. 2019 Mar 6;17(5):4277–4284. doi: 10.3892/ol.2019.10119

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Copyright: © Zhao et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 7. — Cellular pathway of the effects of MET + PTX-induced growth inhibition and apoptosis of PCa cells. MET + PTX increased oxidative stress, and decreased MMP and ATP levels in PCa cells. MET + PTX upregulated the production of P53, PARP, capase3/9, Bax, Cyto-C, and downregulated the production of Bcl-2, promoting the release of Cyto-C, increasing caspase-3/7 activities, and potentiating apoptosis in PCa cells. Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma 2; CytoC, cytochrome c; MET, metformin; MMP, mitochondrial membrane potential; PARP, poly (ADP-ribose) polymerase; PCa, prostate cancer; PTX, paclitaxel.