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Mitochondria supply metabolites for epigenetic modifications and other nuclear\u2010associated activities and certain mitochondrial proteins were found in the nucleus. The voltage\u2010dependent anion channel 1 (VDAC1), localized at the outer mitochondrial membrane (OMM) is a central protein in controlling energy production, cell growth, Ca<jats:sup>2+<\/jats:sup> homeostasis, and apoptosis. To alter the cross\u2010talk between the mitochondria and the nucleus, we used specific siRNA to silence the expression of VDAC1 in glioblastoma (GBM) U87\u2010MG and U118\u2010MG cell\u2010derived tumors, and then monitored the nuclear localization of mitochondrial proteins and the methylation and acetylation of histones. Depletion of VDAC1 from tumor cells reduced metabolism, leading to inhibition of tumor growth, and several tumor\u2010associated processes and signaling pathways linked to cancer development. In addition, we demonstrate that certain mitochondrial pro\u2010apoptotic proteins such as caspases 3, 8, and 9, and p53 were unexpectedly overexpressed in tumors, suggesting that they possess additional non\u2010apoptotic functions. VDAC1 depletion and metabolic reprograming altered their expression levels and subcellular localization, specifically their translocation to the nucleus. In addition, VDAC1 depletion also leads to epigenetic modifications of histone acetylation and methylation, suggesting that the interchange between metabolism and cancer signaling pathways involves mitochondria\u2010nucleus cross\u2010talk. 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