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The metabolism in tumor cells shifts from oxidative phosphorylation to glycolysis even in an aerobic environment. This phenomenon is known as the Warburg effect. This effect is regulated mainly by polypyrimidine tract‐binding protein 1 (  PTBP 1 ), which is a splicer of the m RNA  for the rate‐limiting enzymes of glycolysis, pyruvate kinase muscle 1 and 2 ( PKM 1 and  PKM 2). In the present study, we demonstrated that miR‐133b reduced  PTBP 1 expression at translational level and that the expression levels of miR‐133b were significantly downregulated in gastric cancer clinical samples and human cell lines, whereas the protein expression level of  PTBP 1 was upregulated in 80% of the 20 clinical samples of gastric cancer examined. Ectopic expression of miR‐133b and knockdown of   PTBP 1  in gastric cancer cells inhibited cell proliferation through the induction of autophagy by the switching of  PKM  isoform expression from  PKM 2‐dominant to  PKM 1‐dominant. The growth inhibition was partially canceled by an autophagy inhibitor 3‐ MA  or a reactive oxygen species scavenger  N ‐acetylcysteine. These findings indicated that miR‐133b acted as a tumor‐suppressor through negative regulation of the Warburg effect in gastric cancer cells.

MiR‐133b inhibits growth of human gastric cancer cells by silencing pyruvate kinase muscle‐splicer polypyrimidine tract‐binding protein 1