Transcriptomics analysis and redox-dependent metabolic rewiring in triple-negative breast cancer cells

Glucose metabolism toward aerobic glycolysis provides cancer cells with a rapid generation of pyruvate, ATP, and NADH. CtPB2, an NADH-dependent transcriptional co-regulator, has been proposed to work as an NADH sensor, linking metabolism to transcriptional reprogramming. Here we described how the down-regulation of CtBP2 strongly reduces cell proliferation in triple negative breast cancer (BC) cell line, by modulating several intracellular pathways also through gene expression modification. Our data highlight the critical role of NADH in controlling energetic and anabolic demands in cancer cells. In this work, we analyzed as two-color hybridizations using Agilent Technologies whole human genome 4x44K microarrays, the Gene expression profiles (GEP) modification regulated by CtPB2 in MDA-MB-231 breast cancer cell line. Samples were named as follows: shCtBP2 cells (CtBP2 silencing in MDA-MB231 cancer cells by stable RNA interference of CtBP2); HIPP (small CtBP2 inhibitor) and P4 (small CtBP2 inhibitor), all compared to control sample represented by untreated MDA-MB-231 BC cell line.