Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0086872
Title: MiR-122 targets pyruvate kinase M2 and affects metabolism of hepatocellular carcinoma
Authors: Liu, A.M. 
Xu, Z.
Shek, F.H.
Wong, K.-F. 
Lee, N.P.
Poon, R.T.
Chen, J.
Luk, J.M.
Issue Date: 23-Jan-2014
Citation: Liu, A.M., Xu, Z., Shek, F.H., Wong, K.-F., Lee, N.P., Poon, R.T., Chen, J., Luk, J.M. (2014-01-23). MiR-122 targets pyruvate kinase M2 and affects metabolism of hepatocellular carcinoma. PLoS ONE 9 (1) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0086872
Abstract: In contrast to normal differentiated cells that depend on mitochondrial oxidative phosphorylation for energy production, cancer cells have evolved to utilize aerobic glycolysis (Warburg's effect), with benefit of providing intermediates for biomass production. MicroRNA-122 (miR-122) is highly expressed in normal liver tissue regulating a wide variety of biological processes including cellular metabolism, but is reduced in hepatocellular carcinoma (HCC). Overexpression of miR-122 was shown to inhibit cancer cell proliferation, metastasis, and increase chemosensitivity, but its functions in cancer metabolism remains unknown. The present study aims to identify the miR-122 targeted genes and to investigate the associated regulatory mechanisms in HCC metabolism. We found the ectopic overexpression of miR-122 affected metabolic activities of HCC cells, evidenced by the reduced lactate production and increased oxygen consumption. Integrated gene expression analysis in a cohort of 94 HCC tissues revealed miR-122 level tightly associated with a battery of glycolytic genes, in which pyruvate kinase (PK ) gene showed the strongest anti-correlation coefficient (Pearson r = -0.6938, p =
Source Title: PLoS ONE
URI: http://scholarbank.nus.edu.sg/handle/10635/109467
ISSN: 19326203
DOI: 10.1371/journal.pone.0086872
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