AI Article Synopsis

  • - The study finds that miR-448 is elevated in gastric cancer (GC) samples and contributes to cancer cell growth by enhancing glycolysis.
  • - miR-448 targets KDM2B, which normally helps regulate metabolism; when miR-448 is overexpressed, it reduces KDM2B levels, leading to increased glycolytic activity and decreased oxidative phosphorylation.
  • - The research links high levels of miR-448 in GC tissues to poor patient outcomes and suggests a new understanding of metabolic regulation in cancer, which could be targeted for therapy.

Article Abstract

MicroRNAs are critical in various human cancers, including gastric cancer (GC). However, the mechanism underlying the GC development remains elusive. In this study, we demonstrate that miR-448 is increased in GC samples and cell lines. Overexpression of miR-448 facilitated the proliferation of GC cells by stimulating glycolysis. Mechanistically, we identified KDM2B, a reader for methylated CpGs, as the target of miR-448 that represses glycolysis and promotes oxidative phosphorylation. Overexpression of miR-448 reduced both the mRNA and protein levels of KDM2B, whereas KDM2B re-expression abrogated the miR-448-mediated glycolytic activities. Furthermore, we discovered Myc as a key target of KDM2B that controls metabolic switch in GC. Importantly, a cohort of 81 GC tissues revealed that miR-448 level closely associated with a battery of glycolytic genes, in which KDM2B showed the strongest anti-correlation coefficient. In addition, enhanced miR-448 level was significantly associated with poor clinical outcomes of GC patients. Hence, we identified a previously unappreciated mechanism by which miR-448 orchestrate epigenetic, transcriptional and metabolic networks to promote GC progression, suggesting the possibility of therapeutic intervention against cancer metabolic pathways.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008346PMC
http://dx.doi.org/10.18632/oncotarget.8020DOI Listing

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