Rapamycin suppresses small bowel adenocarcinoma HUTU 80 cells proliferation by inhibiting hypoxia-inducible factor-1α mediated metabolic reprogramming

Figure 6 Rapamycin inhibited glycolysis in HUTU 80 cells via inhibition of the mammalian target of rapamycin/hypoxia-inducible facto-1α pathway. A: Measurement of glucose consumption, lactate production and adenosine triphosphate generation to reflect the glycolytic metabolism of HUTU 80 cells; B: Protein levels were assayed after treatment of HUTU 80 cells with rapamycin, including mammalian target of rapamycin (mTOR), eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) and 70 kDa ribosomal protein S6 kinase (p70S6k), phosphorylated (p)-mTOR, p-4E-BP1 and p-p70S6k and hypoxia-inducible facto-1α; C: Quantification of protein expression using ImageJ. Data are presented as the mean ± SD (n = 3). ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. HIF-1α: Hypoxia-inducible factor-1α; ns: No significance; RAPA: Rapamycin; ATP: Adenosine triphosphate; mTOR: Mammalian target of rapamycin; p-mTOR: Phosphorylated-mammalian target of rapamycin; 4E-BP1: Eukaryotic translation initiation factor 4E-binding protein 1; p-4E-BP1: Phosphorylated-eukaryotic translation initiation factor 4E-binding protein 1; p70S6k: 70 kDa ribosomal protein S6 kinase; p-p70S6k: Phosphorylated-70 kDa ribosomal protein S6 kinase.