All of the other genes that regulated by NANOG and miRNAs are known to be related with stem cells. To further verify our results, we performed analysis of function categories with these ten targets in PIR and found that they are development proteins and related with transcription regulation. Our results clearly reveal the effects of epigenetic regulations on the development of ESCs in biological networks, findings which are consistent with previous studies performed using molecular and cell technology. This finding may provide candidate pathway for deep detection about ESCs molecular mechanism from post transcriptional level. Mitochondria are the sites of vital cellular functions such as the synthesis of the cellular energy by oxidative phosphorylation, the tricarboxylic acid cycle, amino acid, and heme biosynthesis. Deleterious mitochondrial DNA mutations have been reported to cause a broad spectrum of cellular and organismal responses including apoptosis, carcinogenesis, aging and neurological degeneration, and are an important cause of inherited disease. For example, mtDNA missense mutations have been associated with ophthalmological and neurological diseases known as Leber’s Hereditary Optic Neuropathy, and Neurogenic muscle weakness, Ataxia and Retinitis Pigmentosa. Transfer RNA mutations are now known for Myoclonic Epilepsy and Ragged-Red Fiber Disease ; Mitochondrial Encephalomyopathy, Lactic Acidosis, and Strokelike Symptoms ; and Maternally Inherited Myopathy and Cardiomyopathy. Another frequently described pathology associated with reduced mtDNA content is mtDNA depletion syndromes, a group of severe diseases of childhood. The affected persons usually suffer from quantitative decrease in copy number of mtDNA with progressive pathophysiological PR-171 Proteasome inhibitor disorders and subsequent death in their first year of life. To date, over 100 heritable disorders have been attributed to defects in mitochondrial function in humans, and new mitochondrial disease genes are still being identified. Human mtDNA contains one single control region called the Dloop that controls mtDNA replication and transcription of mtDNA-encoded OXPHOS genes, Mutation in the D-loop region is a universal feature and has been reported in all tumors examined to date. Mutations in the D-loop region result in altered binding affinities of the nuclear proteins involved in mtDNA replication and transcription leading to the depletion of mtDNA content. Consistent with this notion, our laboratory recently reported a near absence of mtDNA-encoded cytchrome coxidase subunit II expression in more than 40% of breast and ovarian tumors. Other laboratories measured mtDNA directly in paired normal and tumors and reported a decrease in mtDNA content in breast, renal, hepatocellular, gastric and prostate tumors. Reduced mtDNA is shown to decrease mtOXPHOS activity in renal tumors. A study also demonstrated that decrease in mtDNA content correlates with tumor progression and prognosis in breast cancer patients. Indeed our studies demonstrate that reduced mtDNA content leads to tumorigenic phenotype in vitro. These studies suggest that mtDNA homeostasis plays an important role in tumorigenesis and may contribute to Warburg effect.