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Background  There exists a general recognition of the fact that mitochondrial remodelling as a result of aerobic glycolysis ensures human somatic cells to revert to a more primitive-form exhibiting stem-like phenotype. The present study is an attempt to demonstrate that miR-2909 RNomics within human peripheral blood mononuclear cells (PBMCs) has the inherent capacity to re-program these cells to exhibit mitochondrial remodelling paralleled by aerobic glycolysis together with intracellular lipid inclusions. Such re-programmed PBMCs also expressed genes having ability to sustain their de-differentiation state and survival.    Material and methods  Human PBMCs were programed to ectopically express miR-2909. Expression levels of genes including glucose transporter-1 ( Glut-1) , hexokinase ( HK) , hypoxia inducia factor-1  (HIF-1α) ,  c-Myc ,  p53 ,mechanistic target of rapamycin complex  (mTORC1 ), polycombcomplex protein ( Bmi-1) ,  Notch , Nanog , Tie-2 ,  Oct-4 , CD59 ,  p53 ,  CD34 , B-cell lymphoma-2 ( Bcl2) ,sterol regulatory element-binding protein2 ( SREBP2 ), peroxisome proliferator-activated receptor gamma  (PPARγ ) nuclear respiratory factor 1 ( NRF1 ), mitochondrial transcription factor A ( Tfam ), peroxisome proliferator-activated receptor gamma coactivator 1-alpha ( PGC1α ) within miR-2909 expression vector transfected human PBMCs as well as PBMCs transfected with control vector containing scrambled sequence after 48h post-transfection using RT-qPCR and cellular ultrastructural features induced by miR-2909 ectopic expression were observed using transmission electron microscopy and morphometric analysis of an electron micrograph.    Results  Ectopic expression of miR-2909 within human PBMCs resulted in their reprogramming into stem-like phenotype indicated by mitochondrial globular shaped coupled with cristae-poor morphology. Nuclear to cytoplasmic ratio (N/C), quantification of ATP levels, GSSG/GSH ratio, mitochondrial cytochrome  c  oxidase activity, secreted lactate concentrations, activity of antioxidant enzymes, levels of esterified cholesterol and triglycerides and flow-cytometric detection of apoptosis confirmed the compromised nature of mitochondrial function induced by ectopic miR-2909 expression in human PBMCs.    Conclusion  Based upon these results we propose that AATF gene-encoded miR-2909 may act as an epigenetic switch for cellular aerobic-glycolysis to ensure de-differentiation.

Human cellular mitochondrial remodelling is governed by miR-2909 RNomics