miRNA expression profiling of HCT116 cell after dichloroacetate treatment

Using the highly sensitive miRNA array, we screened out different microRNAs regulated by different concertration of dichloroacetate for different time. Among them 119 microRNAs were obvious Metabolic abnormality is one of the hallmarks of cancer and has been shown to be involved in chemoresistance. In this context, targeting the abnormal metabolism of cancer cells has been an intense avenue of research aiming at asphyxiating the tumor . DCA inhibits the enzymatic activity of Pyruvate Dehydrogenase Kinases (PDK 1 to 4), which are enzymes critical for the activation of the pyruvate dehydrogenase necessary to transform pyruvate into acetyl-CoA, linking the glycolytic metabolism to the citric acid cycle. DCA is primarily used to treat lactic acidosis and hereditary mitochondrial disease, which has been also reported to have anti-cancer effect . However, the mechanism underlying the effect of DCA on CRC treatment remain unsettled. Multiple and complex mechanisms have been described that control the metabolic shift in cancer cells, including microRNAs (miRNAs). MicroRNAs represents a class of small endogenous noncoding RNAs that regulate translation and degradation of mRNAs. Besides controlling the metabolism, miRNAs participate in many more biological processes including cell proliferation, migration, apoptosis , self-renewal, initiation and development of cancers, and chemoresistance.Here we explore the molecular mechanism involved in regulating glucose metabolism and associated chemotherapy resistance in CRC. By exploiting DCA, pyruvate dehydrogenase kinase (PDK) inhibitor, in CRC cells, trying to elucidate the roles of related miRNAs and thereby outlining a signaling pathway. In this study, HCT116 cell was treated with different contrations of dichloroacetate (5mM, 10mM, 20mM) for different times (12h, 24h,48h)